Increased activity of LCAT has been observed in metabolic syndrome and suggested to be a marker of subclinical atherosclerosis, indicating that elevated LCAT is not necessarily beneficial for cardioprotection [101], and other studies on Type 2 diabetes subjects indicate that increased LCAT activity may contribute to impaired or reduced antioxidative functionality of HDL [102]. The gene discussed is LCAT; the disease is type 2 diabetes mellitus.