Our data suggest that RA-patients with wild-type polymorphisms could potentially benefit from concomitant MDR1-inhibition (such as by cyclosporine, tacrolimus, and hydroxychloroquine [3]), administration of GC analogues that are less sensitive to P-gp transport (or not a substrate for P-gp), or treatments that are not influenced by P-gp, e.g., extracellular acting treatments, such as tumor necrosis factor alpha inhibitors. Here, PGP is linked to rheumatoid arthritis.