Meanwhile, Ttr and Faim were found to be significantly down-regulated in SHRs (Figs. 6D and 6E), where Ttr mutation was strongly associated in amyloidosis, a genetic disorder characterized in many forms such as amyloid cardiomyopathy amyloid, familial amyloid polyneuropathy, leptomeningeal amyloidosis (Faria et al., 2015; Gertz et al., 2015; Gonzalez-Lopez et al., 2015; Lobato et al., 2003; Palaninathan, 2012) and senile amyloidosis (typical pulmonary lesions) (Kruczak et al., 2013). Here, TTR is linked to hereditary disease.