CDKN2A and neoplasm: To our knowledge, c-MYC and its co-factor, BMI1, as key transcription factors, are responsible for regulating the expression of key tumor-related genes such as p16. A possible mechanism for the collaboration of c-MYC and BMI1 was suggested by studies demonstrating that BMI1 inhibits c-MYC-induced apoptosis through p16 repression [39].