The activated JAK/STAT signaling drives increased expression and activity of ADAR-1, which contributes to the malignant reprogramming of myeloid progenitors into LSC and CML development, as well as enhanced MDM2 expression and inhibition of the P53 tumor suppressor by creating misspliced isoforms of glycogen synthase kinase 3 beta (GSK3) [122]. This evidence concerns the gene TP53 and chronic myelogenous leukemia, BCR-ABL1 positive.