Collectively, these results (i) indicate a critical role of TNFα/TNFR2 signaling in the protection of the skin against oxidative stress, (ii) might explain the appearance of psoriasis and lichen planus in patients treated with anti-TNFα therapies [5]–[10], and (iii) support the idea that specific inhibition of the TNFα/TNFR1 signaling axis while leaving TNFα/TNFR2 signaling unaffected would inhibit the pathological effects of TNFα and reduce the side effects associated with this therapy [19],[36]. The gene discussed is TNFRSF1A; the disease is psoriasis.