Indeed, using CRISPR-Cas9 editing to disrupt the interaction between ZFP423-EBF2 induced extensive “browning.” When ZFP423 was lost in adipocytes, an EBF2 NuRD-to-BAF coregulator switched and a shift of PPARγ occupancy to thermogenic genes formed (Shao et al. 2016; Shao et al. 2021b), providing a potential therapeutic target for fighting obesity. Here, ZNF423 is linked to obesity due to melanocortin 4 receptor deficiency.