Prior reports have demonstrated a complex regulation of BMI-1 activation via phosphorylation, since AKT-mediated phosphorylation of BMI-1 could modulate its function in a Ink4a/Arf-independent [53] or dependent manner [61], to make BMI-1 an oncogene or a tumor suppressor gene, respectively, with opposing effects on cancer outcome. The gene discussed is CDKN2A; the disease is neoplasm.