Rainwater et al. attributed their findings to the presumption, nonenzymatic glycosylation of Apo(a) in type 2 diabetic patients increases the size of the molecule, which may be responsible for lower plasma Lp(a) levels in type 2 diabetics as there is inverse relationship between Apo(a) size and plasma Lp(a) [26,27]. Here, LPA is linked to type 2 diabetes mellitus.