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Plasma cholesterol levels, the lipoprotein distribution, blood cell counts, and hepatic expression of lipoprotein receptors, including SR-BI, LDL receptor 17-AAG mw (LDLr), and LDLr related protein 1 (LRP1) were determined. Moreover, VLDL production, serum decay and liver uptake of [3H]-cholesteryl ether-labeled HDL, hepatobiliary and fecal cholesterol secretion, and macrophage RCT were analyzed. In addition, tissue macrophage cholesterol homeostasis and atherosclerosis susceptibility were examined by Oil-red-O staining and immunohistochemical staining against Moma-2. To analyze the potential synergistic role of ABCA1 and SR-BI in the RCT process, we generated ABCA1/SR-BI dKO mice. The absence of ABCA1 and SR-BI in the dKO mice was verified at DNA level by performing PCR on genomic DNA (Supplementary Fig. 1). From the crosses of ABCA1/SR-BI double heterozygous mice, 7.2%, 6.5%, and 6.2% of the offspring were ABCA1 KO, SR-BI KO, and dKO mice, which are close to the expected Mendelian inheritance rate of 6.25%. Homozygous dKO males are fertile while dKO females, similar to SR-BI KO females [18]?and?[19], are infertile, which could be reversed by administering the cholesterol-lowering drug probucol. However, as described for ABCA1 KO mice [20], also under these conditions a lower frequency of pregnancy and extensive neonatal Microtubule Associated inhibitor death of pups born from dKO mothers was observed. No significant differences in body weight between wild-type (WT), ABCA1 KO, SR-BI KO, and dKO mice were observed at the age of 12 weeks (22.7?��?0.9?g, 20.3?��?0.3?g, 22.0?��?0.6?g, 21.3?��?0.3?g, respectively). Furthermore, dKO mice born from ABCA1?��?SR-BI double tiospirone heterozygous breedings did not appear to have a reduced life expectancy as they can reach ages of >1 year. In line with previous studies [8], [9], [18]?and?[19], SR-BI KO mice showed increased plasma free (5.5-fold, p?80% and >99% decrease in the plasma TC and HDL-C levels, respectively ( Fig. 1A�CC). Of note, ABCA1 deficiency dramatically reduced the plasma free cholesterol levels (22-fold, p?