AKT1 and neoplasm: As a core ECM component, FN1—following secretion by scPAS + cells and CAFs—participates in resistance through dual mechanisms: first, constructing “endothelial-tumor cell” adhesion bridges whereby FN1 simultaneously binds integrin α5β1 on endothelial surfaces and integrin αvβ3 on tumor cell surfaces, enhancing scPAS + cell vascular wall anchoring and reducing tumor cell detachment and apoptosis following TACE treatment; second, activating PI3K/Akt pathways in endothelial cells, upregulating MMP9 expression and promoting vascular wall remodeling, providing invasion and metastasis channels.