MyD88-dependent pathway activates NF-κB and mitogen-activated protein kinase (MAPK) for induction of inflammatory cytokine genes, while TRIF-dependent pathway promotes an alternative pathway leading to the activation of IRF3, NF-κB, and MAPKs for induction of type I IFN and inflammatory cytokine genes.57 The TRIF-dependent pathway also mediates the expansion and functional exhaustion of HSPCs in sepsis.55,56. The gene discussed is NFKB1; the disease is Sepsis.