This binding not only impairs macrophage receptor with collagenous structure (MARCO)-mediated bacterial clearance and phagocytosis but also activates tumor necrosis factor (TNF)-α secretion, which has an indirect impact on the exaggeration of the inflammatory response and thereby the spread of sepsis, as documented by enhanced survival and less pronounced sepsis in FcRγ−/− mice compared to in wild type (WT) mice [42,43]. Here, FCER1G is linked to Sepsis.