TP53 and acute lymphoblastic leukemia: AICAR-mediated AMPK activation was found to be a proficient cytotoxic agent in Acute lymphoblastic leukemia (ALL) cells and the mechanism of its anti-proliferative and apoptotic effect appear to be mediated via activation of p38-MAPK pathway, increased expression of cell cycle inhibitory proteins p27 and p53, and downstream effects on the mTOR pathway, hence exhibiting therapeutic potential as a molecular target for the treatment of childhood ALL [137].