As the function and expression of both L-type Ca2+ channels [70,71] and TRPC6 [72] have been reported to be upregulated in hypertensive rats, it is intriguing to speculate that these mutual interactions of TMEM16A with other vascular ion channels function cooperatively to augment vasoconstriction and hence increase blood pressure in hypertension. This evidence concerns the gene ANO1 and hypertensive disorder.