In primary CD34+ mononuclear cells obtained from chronic myeloid leukemia (CML) patients, molecular or pharmacologic inhibition of SphK1/S1PR2 signaling enhanced imatinib- or nilotinib-induced growth inhibition [149], indicating the proliferation-promoting role of the sphingolipid network and specifically S1PR2 in these type of hemopoietic progenitor cells. Here, SPHK1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.