Although, it could not be ruled out experimentally that in this case a specific CDKN2A/B and MTAP deletion or epigenetic silence of these TSGs were not present ab initio and at relapse in the leukemia cells of the patient, it is possible to consider that in the CNS microenvironment, but not in the medullar microenvironment, CDKN2A/B/MTAP loss and down-regulation contributed to expansion of the patients neoplastic clone, therefore reinforcing the view that chromosomal deletions encompassing these genes are important for glioma progression. This evidence concerns the gene CDKN2A and central nervous system cancer.