This study supports that altering gene expression of Hoxa11 and Hoxd11 may be a way to grow taller as those genes can turn short bones into long bones.  Unfortunately, the genes that are known to interact with these genes are small in number and not known to be manipulatible by exercise or nutrition.  So it is more likely that in the future the Hoxa11 and Hoxd11 genes may contribute to height growth by manipulating the expression of these genes via an adenovirus.

The pisiform growth plate is lost in humans and supports a role for Hox in growth plate formation.

“The human pisiform is a small, nodular, although functionally significant, bone of the wrist. In most other mammals, including apes and Australopithecus afarensis, pisiforms are elongate. the typical mammalian pisiform forms from two ossification centers. We hypothesize that: (i) the presence of a secondary ossification center in mammalian pisiforms indicates the existence of a growth plate; and (ii) human pisiform reduction results from growth plate loss. We surveyed African ape pisiform ossification and confirmed the presence of a late-forming secondary ossification center in chimpanzees and gorillas. Identification of the initial ossification center occurs substantially earlier in apes relative to humans, raising questions concerning the homology of the human pisiform and the two mammalian ossification centers. Second, we conducted histological and immunohistochemical analyses of pisiform ossification in mice. We confirm the presence of two ossification centers separated by organized columnar and hypertrophic chondrocyte zones. Flattened chondrocytes were highly mitotic, indicating the presence of a growth plate. Hox genes have been proposed to play a fundamental role in growth plate patterning. The existence of a pisiform growth plate presents an interesting test case for the association between Hox expression and growth plate formation, and could explain the severe effects on the pisiform observed in Hoxa11 and Hoxd11 knockout mice. Hoxd11 is expressed adjacent to the pisiform in late-stage embryonic mouse limbs supporting a role for Hox genes in growth plate specification.”

“Compared with humans, the pisiform of most other mammals, including primates, is substantially enlarged and elongated”

Here’s a good visual of growth plate formation:

“a) At birth (P0) the pisiform largely consists of undifferentiated hyaline cartilage. Note the future articular surfaces adjacent to the triquetral (right) and the transitional region near the insertion of the FCU (left). Each of these is distinct from the fibrous periosteal layers that surround the future pisiform shaft. (b) At P4 the cartilage has undergone differentiation to flattened columnar and hypertrophic chondrocytes. It is the calcified hypertrophic matrix that is staining red in Fig. 3(a). (c) By P7 the primary center of ossification begins to be replaced by bone. A broad region of flattened columnar and hypertrophic chondrocytes is preserved at the palmar end (right). (d) At P9 the preserved strip of cartilage displays all of the hallmarks of a growth plate: organized columnar and hypertrophic zones and a perichondrial ring (yellow arrowhead) adjacent to the bone collar. (e) A transverse section through the carpal tunnel demonstrates the unique ossification of the pisiform (left). Note the preserved region of red stained cartilage at the palmar end. In contrast the scapholunate (right) has ossified as a single primary center extending into the projecting tubercle. (f) At P17 the growth plate appears to be losing its activity, as there is no longer an identifiable hypertrophic zone underlying the columnar chondrocytes.”<-so if via LSJL we can induce regions of hyaline cartilage they could potentially become growth plates.

“Full deletion of Hoxa11 or Hoxd11 results in a highly penetrant phenotype with shortened pisiforms that often fuse to the triquetral (ulnare) or less commonly to the scapholunate and triquetral ”

” ‘no Hoxd land’ for short bone morphology”<-Maybe we could upregulate Hoxd in short bones to make them become long bones?

“In short bones and epiphyses, the initial process of chondrocyte differentiation is similar. However, expanded cartilaginous growth plates or active perichondrial rings do not form. Instead, the periphery of these regions largely consists of a narrow three to four cell layer of round chondrocytes that anticipate the future articular zone. In each of these respects (organized chondrocyte zones, active perichondrial ring and deposition of the bone collar), the pisiform is more similar to long bones”<-The organized chondrocyte zones, active perichondrial ring and deposition of the bone collar could be related to Hoxd.

“mice with reduced Hoxa11/Hoxd11 expression display decreased proliferation within mesenchymal condensations and dramatic shortening of the radius and ulna such that they also resemble short bones”

If we can induce Hoxd11 expression in short bones we can make those bones longer and thus ourselves taller.

Looking at the String Embl gene interaction reveals a problem in that very few genes directly interact with Hoxd11.  Although LSJL upregulates the related gene Hoxd10:

Similarly with Hoxa11: