Moreover, by engaging in protein-protein interactions with other transcription factors as a GOF, some cancer-associated p53 mutants were shown with capability of blocking autophagy indirectly by activating several growth factor receptors, such as TGFBR, EGFR, IGFR (95), contributing to sustained active PI3K/Akt/mTOR signaling that subsequently repress autophagy. The gene discussed is TP53; the disease is cancer.