The increased secretion of circulating pro-inflammatory molecules, such as MMP-2, sTNF-R1, and IL-26, the master regulator of inflammation in the non-responder, provides further evidence of the senescence-associated secretory phenotype (SASP) [46] and suggests immunosenescence may be a critical driver of treatment outcome in antibiotic refractory CDI patients receiving FMT. This evidence concerns the gene MMP2 and clostridium difficile infection.