In light of the significantly increased plasma UC/TC ratio and diet-induced transformation of abnormal VLDL-sized lipoprotein particles in Srb1/Ldlr-/- mice, it is reasonable to hypothesize that impeded LCAT activity and presence of Lp-Xs might be the underlying mechanism for the atherosclerotic dyslipidemia and LPG-like nephropathy in Srb1/Ldlr-/- mice, which however need to be defined in future. The gene discussed is LCAT; the disease is kidney disorder.