Our data suggest that directly inhibiting TMEM16A (Figure 6) or manipulating the [Cl–]i gradient to make it become hyperpolarizing rather than depolarizing in pericytes (Figure 4H) are both strategies worth pursuing in order to reduce the deleterious activation of Cav channels that leads to profound capillary constriction and an ensuing decrease of microvascular blood flow, occlusion of capillaries by neutrophils and platelets, cerebral infarction, and hypoxia (Figures 7–9). This evidence concerns the gene ANO1 and cerebral infarction.