The involvement of MafA and MAFB is supported by the loss of MafA in obese mouse models (45–47), high sensitivity of MAFA and MAFB to various islet cell stressors (e.g., high glucose and cytokines; refs. 48, 49), their reduction in T2D islets (34, 50), and compromised GSIS with MAFB depletion in human EndoC-βH1 cells (6) and islets (35). Here, MAFA is linked to type 2 diabetes mellitus.