Mechanistically, KDM6A knockout abolished NGF-induced activation (phosphorylation) of Akt and ERK1/2 (Figure 6C), which are known to be involved in NGF-mediated protection of CML cells against imatinib 23, whereas re-expression of wild-type KDM6A or introduction of the KDM6A-ED mutant re-enabled NGF to trigger activation of Akt and ERK1/2 in K562 cells with KDM6A knocked out (Figure 6D). Here, AKT1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.