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. This evidence concerns the gene LDLR and obesity due to melanocortin 4 receptor deficiency.