ITPR1 and Hepatic fibrosis: Because intracellular/mitochondrial Ca2+ is necessary to maintain the aHSC phenotype (proliferation, αSMA expression, contraction), and because dmXeB potently and specifically blocks IP3R-mediated Ca2+ signaling, we evaluated the capacity of dmXeB to inhibit HSC activation and thus to be a candidate drug to treat liver fibrosis.