Pharmacological inhibition of TMEM16A reduced the ischemia-evoked contraction and death of pericytes, improved postischemic CBF, decreased capillary neutrophil blocks at pericyte somata, and reduced brain hypoxia and infarct size after ischemia, thus highlighting TMEM16A inhibition as a therapeutic strategy to improve reflow after stroke and other conditions of impaired microvascular blood flow. The gene discussed is ANO1; the disease is Stroke.