Upregulation of DYRK2 in CML through VK3-mediated SIAH2 inhibition was further supported by biochemical assays: (a) VK3 treatment induced upregulation of prolyl hydroxylase domain 3 (PHD3), a known SIAH2 target, in addition to DYRK2; (b) c-MYC depletion was caused by VK3-mediated upregulation of DYRK2 and thus was lost by knocking out the DYRK2 gene via CRISPR/CAS9 technology; and (c) incubation of CML cells with VK3 decreased the level of ubiquitinated DYRK2. This evidence concerns the gene EGLN3 and chronic myelogenous leukemia, BCR-ABL1 positive.