TP53 and acute lymphoblastic leukemia: In order to prove that abnormal hypermethylation of genes implicated in the TP53 pathway could be responsible at least in part for the resistance to apoptosis in ALL, TOM-1 and NALM-20 cells were treated with either a demethylating agent (5-aza-2′-deoxycytidine), a caspase-8 activator (Curcumin) that induces apoptosis downstream and independently of p53 and Nutlin-3, an inhibitor of MDM2 and thus an activator of the p53 pathway.