Moreover, deletion of the RvE1 receptor ChemR23 exacerbated aortic valve disease and abolished the beneficial effects of omega-3 PUFA mediated by the transgenic Fat-1 expression, hence reinforcing the idea that the beneficial effects of omega-3 PUFA in aortic valve disease were mediated specifically by the RvE1 and ChemR23 signaling axis, as illustrated in Figure 1 (Artiach et al., 2020a). The gene discussed is CMKLR1; the disease is aortic valve disorder.