Fibrogenesis in S‐ECM samples is likely due to the presence of an activated cancer‐associated fibroblast (CAF) population in the tumor microenvironment, as indicated by the identification of CAF marker genes as key regulators for S‐ECM, including FAP, ACTA2, PDGFRB, VCAN, and ITGA11 [25, 32, 33, 34] (Fig. 4B). The gene discussed is ACTA2; the disease is neoplasm.