The intrinsic chemoresistance of AML blasts is at least partly contributed by CD39-mediated activation of the P2RY13-cAMP-PKA pathway and the ATF4 axis, triggering mitochondrial ROS production and OXPHOS activity that leads to chemoresistance with heightened antioxidant defenses by AML cells (74). This evidence concerns the gene ENTPD1 and acute myeloid leukemia.