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. This evidence concerns the gene VDR and Hyperglycemia.