While we focused on HOXA13 here, it is conceivable that other HOX paralogues are involved in BE pathophysiology, in particular caudal genes such as HOXA10, 11, B13, and C10 are interesting candidates for further investigation, in particular as disruption of collinearity was reported for cluster B in BE9 and in duodenum of murine embryos12. This evidence concerns the gene HOXA13 and Barrett esophagus.