This early surge of circulating TNF-α binds to its corresponding TNF receptor 1 (TNFR1, a specific transmembrane death receptor) to activate immune cells (i.e., macrophages) [2,3] and enhance the release of inflammatory mediators, subsequently leading to the development of a systemic inflammatory response during sepsis [2,3]. Here, TNFRSF1A is linked to Sepsis.