Furthermore, protein-protein interactions with other transcription factors as a GOF and some cancer-associated p53 mutants have been shown the capability to block autophagy indirectly via triggering numerous growth factor receptors as EGFR, TGFBR, and IGFR which contributing to sustain PI3K/Akt/mTOR signaling and subsequently suppress autophagy in cancer (Aschauer and Muller, 2016). The gene discussed is AKT1; the disease is cancer.