What contradicts this hypothesis is that not only HMGCR is downregulated in prostate cancer, but also LDLR. However, mechanisms alternative to LDLR for cholesterol and sterol uptake and efflux have been suggested, including changed activity of SLCO transporters [49] (for example SLCO2B1 is strongly upregulated in the five-study-cohort, Fig. 4a) and modulation to cell-membrane structures like lipid rafts [3, 7, 50]. This evidence concerns the gene LDLR and Familial prostate cancer.