Upon autophagy inhibition, FOXO3a protein increased and accumulated in the nucleus, and transcriptionally activated the pro-apoptotic gene, p53 upregulated modulator of apoptosis, leading to p53-independent apoptosis and consequently sensitizing colorectal cancer (CRC) cells to chemotherapy drugs such as doxorubicin and etoposide[103]. The gene discussed is TP53; the disease is colorectal cancer.