This finding imposed the question of whether non-Ig stimuli can act as a driver of the excessive glomerular C3 deposition (including the subendothelial space), which is characteristic in C3G-affected individuals (16), as well as for the C3 deposition in the renal microvascular endothelium cell lining in aHUS patients (17, 18). This evidence concerns the gene C3 and atypical hemolytic-uremic syndrome.