When we set uncertainty about study quality aside and examine the data we collected as a whole, it is clear that they mirror what we already know from the immunology field.25–27 For example, sequencing results published by Zhang et al35 and Wei et al61 suggest that synovial fibroblasts upregulate a host of inflammatory mediators in RA and OA—some of which, like IL-6 and NGF, we know to be proalgesic. Here, IL6 is linked to rheumatoid arthritis.