Other mechanisms suggested for the pathogenesis of mTOR-inhibitor-induced hypertriglyceridaemia are: (1) an upregulation of the gene CIII A, which is an inhibitor of LPL with a consequent inhibition of TG and VLDL catabolism leading to hypertriglyceridaemia [60]; (2) an upregulation of adipocyte fatty-acid-binding protein expression, which may contribute to hypertriglyceridaemia [78]; and (3) a reduced catabolism of lipoproteins containing apo B 100 leading to an elevation in VLDL concentrations [79]. The gene discussed is LPL; the disease is hypertriglyceridemia.