These mechanical cues can promote YAP1 nuclear translocation via RhoA–FAK–Src signaling, which in turn induces matrix-remodeling and myocontractile programs (e.g., ACTA2/α-SMA, collagens, and fibronectin), enabling CAFs to acquire stable pro-tumor functions such as ECM remodeling, matrix contraction, and metabolic support [107,108]. The gene discussed is YAP1; the disease is neoplasm.