However, Soulillou et al commented that CMAH-/-mice unlikely displayed a universal phenotype that could be extended to humans, and functional lack of LDL receptor predisposes mice to obesity and obesity-associated accelerated AS 46, which indicated that the proposed CMAH-/-LDLR-/-mice model cannot directly reflect the regulation of circulated Neu5Ac on AS progression relating to lipid metabolism disorder and inflammation. Here, LDLR is linked to Obesity.