Notably, hypertriglyceridemia, a core component of TyG index calculation, involves complex molecular pathways including the dysregulation of lipoprotein lipase (LPL) activity and apolipoprotein (Apo) C-II/C-III/A-V function, and angiopoietin-like proteins (ANGPTL3/4/8) mediation, which collectively impair triglyceride clearance and promote atherogenic lipoprotein accumulation (17–20). Here, LPL is linked to hypertriglyceridemia.