Bmi1-deficient mice exhibit neurological disorders, demonstrating the essential role of Bmi1 in regulating the self-renewal of neural stem cells.14, 24, 25 Site-specific phosphorylation of Bmi1 by various kinases influences its tumorigenicity, both positively and negatively, and the phosphorylation of Bmi1 at different serine residues modulates its function through the Ink/Arf pathway.26 Our findings demonstrate that inhibition of Akt Ser473 phosphorylation decreases Bmi1 phosphorylation. The gene discussed is CDKN2A; the disease is nervous system disorder.