TP53 and acute myeloid leukemia: Van Linden demonstrated that the functionality of p53 does not influence the sensitization to antimetabolite chemotherapeutics by Wee1 inhibitors in AML cells and lung cancer cells, suggesting that the use of p53 mutation as a predictive biomarker for response to Wee1 inhibition may be restricted to certain cancers and/or chemotherapeutics, as well as the preclinical data supporting the combination [91].