There are several molecules, including galactose-deficient IgA1 (Gd-IgA1), IgG anti-Gd-IgA1 antibodies, glycan-specific IgG antibodies, and soluble CD89 (an Fc receptor for IgA) that may be implicated in the pathogenesis of IgA nephropathy, the presence of which may portend a greater risk of disease progression and possibly disease recurrence post-transplant (26–32). Here, CD79A is linked to IgA glomerulonephritis.