To investigate the potential role of ApoA-II in lipoprotein particle distribution and progression of AA amyloidosis, we induced AA amyloidosis by co-injection of AA amyloid fibrils (AEF) and AgNO3 (inflammation inducer) in wild type (WT), ApoA-II deficient (Apoa2−/−), ApoA-II overexpressing (Apoa2cTg) and ApoA-I deficient (Apoa1−/−) mice. This evidence concerns the gene APOA2 and AA amyloidosis.