In addition, inhibition of HDAC3 accelerates vascular endothelial proliferation during vascular impairment caused by T2D through activating Nrf2 signaling by inhibiting Keap1 synthesis and Nrf2–Nox4 association, which indicated the potential of HDAC3 as an epigenetic regulator in T2D-related vascular complications (16). Here, KEAP1 is linked to type 2 diabetes mellitus.