Moreover, the current characterized by rottlerin activation and paxilline blockade in vitro, as well as inhibition of fibrosis mediated through BK channel activation in vivo, further support that BK channels may play more important roles than KCa3.1 channels in hepatic fibrosis, at least in models of CCl4-induced liver fibrosis. This evidence concerns the gene KCNN4 and Hepatic fibrosis.