Previous genome-wide association studies (GWASs) of response to TNFi agents in RA have identified the CD84 [6] and PDE3A-SLCO1C1 [7] loci as the strongest candidates but reproducibility has been an issue [8] and recent studies have questioned the utility of studying genetic variation in relation to response to TNFi in RA [9]. The gene discussed is CD84; the disease is rheumatoid arthritis.