The P210BCR−ABL1 also regulates miRNA stability and induces an increase in self-renewal of CML LSCs by mediating the activation of Janus kinase (JAK)/STAT signaling pathway, increasing adenosine deaminases acting on double-strand RNA1 (ADAR1) enzyme levels, which hampers biogenesis of the miR precursor (miR-let7) and increased LIN28B pluripotency gene expression [51, 52]. The gene discussed is SOAT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.