It has been reported that the mechanism may be due to IgA immune complex deposition, mesangial activation and immune system disorders through mucosa-renal axis (Suzuki et al., 2011) and CX3CL1/CX3CR1 axis (Suzuki et al., 2011; Cox et al., 2012) leading to infiltration of inflammatory cells and release of mediators, which ultimately leads to chronic inflammation, glomerular capillary wall damage and red blood cell extravasation, thus resulting in hematuria (Gutierrez et al., 2012a). The gene discussed is CX3CL1; the disease is immune system disorder.