While these findings do not establish a causal role for these complement components in kidney disease progression, these observations represent support in the existing data for the presence of a human failed-repair PTC population expressing high levels of C3, as well as increased inflammatory and pro-fibrotic complement components, such as C3aR1 and CFH, which may contribute to the pro-fibrotic renal microenvironment observed in AKI-to-CKD transition in mouse models. The gene discussed is C3; the disease is kidney disorder.