We propose the following pathway of action of miR-146a: infections or other perturbations activate NF-κB through TRAF6 and other signal transducers; the basal and NF-κB-enhanced levels of miR-146a then limit the amount of TRAF6, allowing the system to quickly return to basal NF-κB activity when the danger has passed; the transient NF-κB activation causes a transient increase in IL-6 and the IL-6 acts on the stem and progenitor cells to transiently promote proliferation and myeloid differentiation. Here, NFKB1 is linked to infection.