KMT2A and acute myeloid leukemia: Given the success of various small molecule inhibitors in specific genetic subtypes of ALL and acute myeloid leukemia (AML) and the improved specificity of next-generation kinase inhibitors [16–20], we performed a kinome-wide domain-specific CRISPR screen in 3 high-risk subtypes of ALL and found that dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) is specifically required for the survival of KMT2A-R ALL.