Namely, the RGX-104 LXR agonist reduced the amount of PMN-MDSCs and M-MDSCs in the tumor site and in the periphery by initiating apoptosis, whereas in ApoE-deficient mice, there was no observable MDSC depletion, indicating that ApoE is necessary for the killing of MDSCs in cooperation with LXR agonism. This evidence concerns the gene APOE and neoplasm.