Since synthesis of non–β cell hormones appears to be negatively regulated by human MAFB (8) and is associated with the loss of β cell identity and activity postnatally in type 2 diabetes (T2D) (10–14), we examined here how MAFA and/or MAFB contributed to this process in adult mice and human islets. The gene discussed is MAFB; the disease is type 2 diabetes mellitus.