Moreover, we determined that DGKα may be a promising therapeutic target in AML, and ritanserin not only negatively regulates SphK1 expression through PLD signaling but also inhibits the Jak-Stat and MAPK signaling pathways via DGKα, providing effective preclinical evidence for ritanserin in the treatment of AML. This evidence concerns the gene SOAT1 and acute myeloid leukemia.