Poggi et al. (2015) reported large deletions in PAR spanning SHOX and CRLF2 in some of the LWD patients, but the common feature among LWD cases is deletions spanning SHOX. Thus, although we cannot exclude that the deletion of CRLF2 is involved in the phenotypic expression of SA, we argue that the similarity to human phenotypes caused by SHOX deficiency support the interpretation that SA is manifested by a reduction of SHOX expression. The deletion of CRLF2 may affect other hitherto unexplored phenotypes in affected horses and possibly also in carriers. This evidence concerns the gene CRLF2 and Leri-Weill dyschondrosteosis.