IgA and anti-epithelial cell antibodies (AECA) bind to the vascular endothelium and promote the migration and activation of neutrophils; this has also been pointed out as one of the causes for the onset of IgAVN.[13] Recent investigations have demonstrated that the concentration of AECA decreases in patients receiving bevacizumab.[14] Moreover, high expression of VEGF was reported in patients with vasculitis and in children with acute-phase IgAV.[15,16] Some reports suggest that bevacizumab administration is unlikely to lead to the development of IgAVN. This evidence concerns the gene CD79A and vasculitis.