DYRK1A and acute myeloid leukemia: First, we identified that pharmacologic DYRK1A inhibition resulted in increased MYC levels via decreased phosphorylation of Thr58 and Ser62 on MYC, which is concordant with a recent publication demonstrating that viral overexpression of DYRK1A in non-KMT2A-R AML results in phosphorylation of Thr58 and Ser62 on MYC and consequently in MYC degradation [38].