When immune cells are first subjected to LPS exposure or undergo TLR activation following an infection: 1) they activate a rapid inflammatory response (increasing the production of TNF-α and other inflammatory mediators); and then, 2) they reprogram their activity and become refractory to further LPS challenge through the influence of various molecular determinants, like IRAK-M overexpression [23], [36]–[38]. This evidence concerns the gene IRAK3 and infection.