FPR2 knockout mice have exacerbated cardiac dysfunction following caecal ligation and puncture in a model of polymicrobial sepsis [152], and RvE1 successfully attenuated polymicrobial sepsis-induced cardiac dysfunction and enhanced bacterial clearance [153], whilst maresin conjugates in tissue regeneration 1 (MCTR1) markedly improved cardiac function in a model of lipopolysaccharide (LPS)-induced cardiac dysfunction [154]. This evidence concerns the gene FPR2 and Sepsis.