NFKB1 and Sepsis: The molecular mechanism behind monocyte reprogramming, in sepsis as well as in cancer, is suggested to rely on a repeated TLR-signal in combination with certain cytokines or mediators (e.g., IL-10, Wnt5a, and PGE2) thus leading to the formation of immunosuppressive NFκB p50:p50 homodimers instead of pro-inflammatory NFκB p65:p50 heterodimers (Figure 5) [13, 26, 120–122].