In this complex scenario, we decided to investigate the expression levels of some genes reported to sustain the BCR-ABL1-independent resistance in CML: in particular, we focused on JAK-STAT, WNT/beta-catenin, and Polycomb pathways, evaluating their de-regulation after 6 months of treatment from diagnosis. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.