To sum up, while there is a growing body of evidence that CaCC TMEM16A contributes to the increased vascular contractility and elevated blood pressure in SHRs, it is currently unclear whether the upregulation of TMEM16A is specific to SHRs or is present in other hypertensive animal models, and further studies will be needed to clarify the molecular mechanisms that regulate TMEM16A activity during hypertension. This evidence concerns the gene ANO1 and hypertensive disorder.