For instance, it has been demonstrated that in the pathogenesis of asthma, an impairment of TNF–TNFR signaling contributes to the polarization toward T helper 2 (Th2) and Th17 phenotypes, raises concentrations of inflammatory cytokines (IL-4, IL-5, IL-17, and TNF) in serum and bronchoalveolar lavage fluid, and exacerbates allergic airway inflammation [11]. Here, TNFRSF1A is linked to asthma.