In fact, Da Dalt et al. demonstrated that PCSK9 KO mice exhibited reduced insulin secretion, glucose intolerance and an increased cholesteryl ester accumulation in β-cells compared with wild-type mice and these alterations were reversed in PCSK9/LDLR double KO mice, suggesting that LDLR mediates cholesterol-induced β-cell dysfunction and insulin resistance by promoting intracellular cholesterol accumulation [32]; moreover, Paquette et al. showed that β-cells are particularly susceptible to cholesterol overload due to their limited capacity for cholesterol efflux [31]. The gene discussed is INS; the disease is Glucose intolerance.