Mice do not express CD89 (but retained to Fcα/μR, for both IgA and IgM), leading to the development of transgenic mice expressing the human CD89 to enable taking this interaction into account whilst studying the role of IgA in vivo, e.g. in (11)IgA nephropathy (12–14), cancer (15) or the inflammatory role of serum IgA (16). This evidence concerns the gene CD79A and IgA glomerulonephritis.