In patients with IgA nephropathy abnormalities in O-glycan biosynthesis result in exposure of the immunogenic Tn antigen by auto-antibodies, resulting in immune complex formation and deposition in the kidneys, leading to kidney failure [29] and it is tempting to think the expression of aberrant O- glycosylation on IgA1 in a similar way could constitute the target of an anti-tumour immune response [30]. This evidence concerns the gene IGHA1 and IgA glomerulonephritis.