Gene editing experiments in human adipocytes showed that an obesity-risk intronic variant of FTO results in higher expression of both IRX3 and IRX5 specifically in adipocyte progenitor cells (Claussnitzer et al., 2015), and deletion of a cis-regulatory module (CRM) harboring the FTO risk variant in mice results in lower Irx3 and Irx5 gene expression in adipocyte progenitors to roughly 70% of control levels (Laber et al., 2021). Here, IRX5 is linked to obesity due to melanocortin 4 receptor deficiency.