Since TP53 mutation is associated with poor treatment response and ASNS expression is associated with ASNase resistance, targeting both mutant p53 and ASNS with APR-246 in combination with ASNase, which depletes circulating asparagine, appears as an attractive strategy that warrants further investigation in ALL, especially in light of the benign safety profile of APR-246 [63]. The gene discussed is TP53; the disease is acute lymphoblastic leukemia.