Mechanistically, using a receptor-interacting protein kinase 3 (RIPK3)-deficient MDSC model, the authors showed that reduced cholesterol in tumour-infiltrating MDSCs led to increased nuclear liver X receptor beta (LXRβ), which in turn forms a heterodimer with retinoid X receptor α (RXRα) thereby directly inducing Arg1 expression via LXRβ-RXRα binding to the Arg1 promoter. Here, RIPK3 is linked to neoplasm.