Once activated, these IRAK kinases initiate a cascade of downstream effects, encompassing the stimulation of nuclear factor-kappa B (NFκB), mitogen-activated protein kinases (MAPKs), and activator protein 1 (AP-1), thereby cementing MyD88's role as a central hub in the inflammatory response15.A number of deactivating mutations within the MyD88 gene have been pinpointed in individuals experiencing recurrent infections caused by pyogenic bacteria16. The gene discussed is NFKB1; the disease is infection.