For example, research has demonstrated that inflammatory tissue priming relies on the intracellular activation of complement C3 and C3a receptors in synovial fibroblasts.18 Additionally, in a mouse model of unilateral ureteral obstruction, complement C3 exacerbates renal interstitial fibrosis by facilitating the M1 macrophage phenotype.19 However, increasing evidence suggests that the C3a exhibits anti-inflammatory properties. This evidence concerns the gene C3 and Ureteral obstruction.