Tamoxifen-mediated GPER activation downregulated RhoA levels, which in turn reduced the phosphorylation of MLC-2 (an actomyosin regulatory protein that controls ECM contractility in HSCs) and also suppressed YAP activation; actinomycin and YAP activation are necessary for the development of fibrosis in HCC tumors [157]. The gene discussed is GPER1; the disease is hepatocellular carcinoma.