Because a previous lineage tracing study has already demonstrated that contribution to the pool of mature α-SMA+ myofibroblasts in the fibrotic murine livers by endothelial cells is rather limited (∼5%), our observation that endothelial deletion of BRG1 attenuates liver fibrosis by as much as 50% (depending on the various measurements) simply cannot be explained by the in vitro data, which suggest that BRG1 promotes the trans-differentiation of endothelial cells into myofibroblast-like cells. Here, ACTA1 is linked to Hepatic fibrosis.