In particular, the C57BL/6j background generally yields to milder phenotypes in a number of disease models, e.g. amyotrophic lateral sclerosis (Heiman-Patterson et al., 2011), autistic spectrum disorder (Kerr et al., 2013), neurokinin-1 receptor knockout mice (McCutcheon et al., 2008), diabetes and insulin resistance (Haluzik et al., 2004), although it has occasionally been found to worsen aspects of the phenotype e.g. motor coordination in a model of Angelman syndrome (Huang et al., 2013) or amyloid plaque load in a mouse model of AD (Lehman et al., 2003). Here, TACR1 is linked to amyloidosis.