Transgenic mice overexpressing murine apoA-II (containing ~4.5 kb of sequence 5′ to the first exon and ~8.5 kb of sequence 3′ to the fourth exon of the mouse ApoA-II gene) had a reduced level of paraoxonase, which decreased the HDL atheroprotective effect and exhibited hypertriglyceridemia, obesity, and atherosclerosis, characteristics associated with the insulin resistance syndrome [66,71,83,84]. Here, APOA2 is linked to hypertriglyceridemia.