In clear contrast, our earlier studies revealed that HDL particles were depleted of CE and of apoA-I and enriched in TG in atherogenic dyslipidemia of insulin-resistant states associated with elevated CETP activity, such as metabolic syndrome and Type 2 diabetes; such compositional alterations were paralleled by reduced antioxidative activity of HDL [40]. The gene discussed is APOA1; the disease is metabolic syndrome.