Interestingly, we demonstrated that the physiological P2RY6 ligand UDP and the specific P2RY6 agonist MRS2693 can restore normal monocyte differentiation through re-induction of AMPK-dependent autophagy in primary myeloid cells from some, but not all, CMML patients (Figure 4). This evidence concerns the gene PRKAA2 and chronic myelomonocytic leukemia.