NUP98 and acute myeloid leukemia: Finally, knockdown of Cdk12 caused a mild but significant impairment of growth of NUP98::KDM5A-driven AML in vivo (Fig. 6E, F), and immunophenotyping of leukemic blasts showed that Cdk12-deficient, iRFP670/CD45.2-positive AML cells displayed reduced levels of the progenitor marker c-Kit, which is in line with their reduced leukemogenic potential (Fig. 6G and Supplementary Fig. 6D, E).