Intriguingly, Franke et al. (2016) further uncovered the pathogenesis of this kind of brachydactyly‐anonychia, suggesting that a new chromatin domain (neo‐TAD) was formed by 17q24.3 duplications which incorporated the next flanking gene, Kcnj2, and resulted in ectopic contacts of Kcnj2 with the Sox9 regulatory region, subsequent misexpression of Kcnj2, and a limb malformation phenotype. This evidence concerns the gene KCNJ2 and brachydactyly.