Goossens et al. (2019) demonstrated that, in ovarian cancer cells, cholesterol depletion from lipid rafts, caused by increased cholesterol efflux due to specific transporters, is responsible for the phenotypic reprogramming of macrophages into tumor-associated macrophages, making them more responsive to pro-tumor signals such as interleukin-4 and more resistant to the action of anti-tumor cytokines such as interferon-gamma [93]. The gene discussed is IL4; the disease is neoplasm.