Further evidence to support this point stems from our previous findings demonstrating that in both BCR::ABL1-positive and-negative leukemia cell lines MEK1/2 inhibition induces the accumulation of tyrosine-phosphorylated endogenous p73 [13], a p53 paralogue that is stabilized and transcriptionally activated at the nuclear level by ABL1-mediated direct phosphorylation at its Tyr99 residue [39], thus indicating that ABL1 can play an important tumor-suppressor role in leukemia. This evidence concerns the gene TP53 and neoplasm.