ACTA1 and neoplasm: HSCs are reportedly a major contributor to liver fibrosis.[27] HSCs are in a resting state in healthy livers; however, when stimulated by inflammation or tumor cells, they can transdifferentiate into myofibroblasts associated with connective tissue proliferative response and tumor development.[14, 15] ICC is a highly fibrous proliferative tumor with a dense stroma rich in α‐SMA‐positive myofibroblasts.[28] Based on the finding that cPKM expression levels are correlated with the degree of fibrosis, we speculated that ICC cells with high cPKM expression promote myofibroblast activation in HSCs.