High levels of ApoC-III are known to contribute to hypertriglyceridemia via the inhibition of (a) the activity of lipoprotein lipases (LPL) and (b) the uptake of TG by the liver [22], thus resulting in an increased half-life of TG-rich lipoproteins; elevated levels of ApoC-II have already been reported in patients with T2DM and obesity [23,24]; however, the biological meaning of differences in ApoC-II levels is yet to be fully elucidated, as this apolipoprotein seems to have LPL-promoting activity [25]. This evidence concerns the gene APOC2 and hypertriglyceridemia.