A recent study in mouse models has shown that the pharmacological inhibition of BRD9 restores β‐cell function and ameliorates hyperglycemia through a ligand‐dependent switch between the vitamin D receptor and BAF remodeling complexes.[57] Besides, BRD9 inhibition limits inflammation by blocking the induction of ISG expression.[15, 16, 17] However, whether the local application of BRD9 degraders or inhibitors could attenuate the sustained inflammatory state of the wound in diabetes remains to be elucidated. The gene discussed is VDR; the disease is diabetes mellitus.