The low percentage of TP53 mutations in ALL patients as well as the resistance to apoptosis suggest that regulation of apoptosis in ALL could be mediated by other mechanisms involved in the abnormal function of the p53 pathway or p53 independent mechanisms, including the deregulation of genes of the BCL2 family such as BCL2, BAX, BCL-XL, mechanisms that should be explored in order to improve our understanding of the pathogenesis of the disease. This evidence concerns the gene BCL2 and acute lymphoblastic leukemia.