In this way, in the absence of KLF4 in CML LSCs, dual specificity tyrosine phosphorylation regulated kinase 2 (DYRK2) was remarkably upregulated, which in turn mediated the activation of P53 and c-MYC, and facilitated proteasomal degradation through phosphorylation, leading to apoptosis and decrease in the self-renewal in CML LSCs [53]. Here, DYRK2 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.