In this way, Morotti et al. showed that PTEN-tail phosphorylation, mediated by BCR-ABL1-activated casein kinase II (CKII), caused a reduction of PTEN phosphatase activity, thus uncovering another inhibition mechanism present in CML [64]. The gene discussed is PTEN; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.