In lung adenocarcinoma models, radiotherapy induces tumor cells to release HMGB1, which activates CAFs through the TLR4/PI3K/AKT pathway—driving conversion to the myCAFs phenotype with upregulated FAP, α‐SMA, and Collagen I expression, thereby enhancing tumor fibrosis and invasiveness [100]. This evidence concerns the gene AKT1 and neoplasm.