The same results were reported by Wahle et al., who showed that the non-selective β-adrenergic receptor antagonist propranolol blocked the inhibitory effect of norepinephrine (at 10−5 M) on IFN-γ production by anti-CD3/CD28-activated T cells in rheumatoid arthritis patients and healthy subjects [13]. This evidence concerns the gene CD28 and rheumatoid arthritis.