Consistently, our in vivo studies on hSOSTki.Col1a2+/G610C.ApoE-/- mice and Δloop3-hSOSTki.Col1a2+/G610C.ApoE-/-mice indicated that loop3 deficiency maintained the suppressive effects of sclerostin on AngII-induced inflammatory responses, as well as AA and atherosclerosis progression. This evidence concerns the gene SOST and atherosclerosis.