Mechanistic studies demonstrate that excessively high LDL-C induces cholesterol overload in renal cells via CD36-mediated endocytosis, activating endoplasmic reticulum stress and the unfolded protein response, which triggers mitochondrial dysfunction and Bax/Bak-dependent apoptosis, ultimately promoting proteinuria and glomerulosclerosis (30–32). The gene discussed is BAK1; the disease is glomerulosclerosis.