Not only that, after stroke, the elevated cytoplasmic Ca2+ concentration in pericytes activates the Ca2+ gated anion channel TMEM16A, causing chloride ions to flow out, the cell membrane to depolarize, and voltage‐gated calcium channels to open, resulting in strong contraction of the pericyte and aggravating the BBB dysfunction, leading to the “no‐reflux phenomenon” after stroke. This evidence concerns the gene ANO1 and stroke disorder.