Although the specific roles of SAA3 in colonic and adipose tissue are not well understood, in consideration of recent studies, it is possible that elevation of SAA3 in mice (and potentially SAA1 in humans) by TLR/MyD88/NF-κB signaling downstream of LPS or other components of the intestinal microbiota represents a facet of the elevated inflammatory tone observed in obesity. Here, NFKB1 is linked to obesity disorder.