Combined overactivation of AKT and MYC in LUAD models synergistically induces squamous markers such as P40, with further augmentation under the selective pressure of EGFR inhibition.38 Similarly, in prostate cancer, the AKT/mTOR pathway has been associated to lineage plasticity, facilitating the transition from AR-dependent adenocarcinoma to AR-independent states like NEPC.68 This transition often follows ADT and is closely linked to resistance mechanisms. The gene discussed is AR; the disease is prostate carcinoma.