Without AKAP150, mouse arteries exhibited vasoconstriction upon acute increases in extracellular D‐glucose and in diabetes.38 CaN anchoring by AKAP150 is required for BK channel impairment during hyperglycaemia and diabetes, which promotes enhanced vascular tone.12 In our study, the function of AKAP150 in the vasculature from STZ‐induced diabetes was undeniable (Figures 1A‐C and 2A,B). This evidence concerns the gene NUP214 and diabetes mellitus.