In the “cardiac arrest group,” it is likely that the release of TNFα as a proapoptotic cytokine was triggered, leading to higher concentrations of TNFα in the skin of the “cardiac arrest group.” However, the role of TNFα is varied and dependent on a wide range of factors, including receptor binding (TNF-R1 vs. TNF-R2), the local cytokine milieu, the presence of reactive oxygen species, as well as many additional factors (88, 89). The gene discussed is TNFRSF1A; the disease is cardiac arrest.