AKT1 and neoplasm: Mechanistically, DDR1 sustained tumor cell survival by forming 14–3-3-mediated assembly of a DDR1/14–3-3/Akt ternary complex, thereby activating the Akt/mTORC1/SREBP1/SCD1 axis to promote monounsaturated fatty acid (MUFA) biosynthesis and suppress ferroptosis.