In other cancers, such as pancreatic and skin carcinomas, premalignant epithelial progenitors carrying mutations in KRAS or HRAS undergo apoptosis in response to TGF-β, and to escape this apoptosis, RAS-mutant cells acquire alterations that inactivate the TGF-β pathway or decouple TGF-β signalling from apoptosis.37,38 This characteristic also differs in iCCA. This evidence concerns the gene HRAS and skin carcinoma.