The experimental data discussed so far are in line with (i) evidence that in global Fpr2 null mice failure to activate this receptor leads to cardiometabolic syndrome, diastolic dysfunction and reduced survival rates with signs of multi-organ non-resolving inflammation (Tourki et al, 2020) and (ii) genomic profiling of RA patient blood. Here, FPR2 is linked to rheumatoid arthritis.