BMI1 has been reported as an oncogene by regulating p16 and p19, which are cell cycle inhibitor genes. BMI1 knockout in mice results in defects in hematopoiesis, skeletal patterning, neurological functions, and development of the cerebellum. It is a component of a Polycomb group (PcG) multiprotein PRC1-like complex, a complex class required to maintain the transcriptionally repressive state of many genes, including Hox genes, throughout development. BMI1 is necessary for efficient self-renewing cell divisions of adult hematopoietic stem cells as well as adult peripheral and central nervous system neural stem cells. BMI1 is also thought to inhibit ageing in neurons through the suppression of p53.