Crucially, it is the response of the Calu‐3 cells to virus infection, via RNA sensing, that drives macrophage activation in these experiments, evidenced by suppression of activation after either MAVS depletion or NF‐κB (TPCA‐1) or JAK inhibition (Ruxolitinib) in the infected Calu‐3 cells. This evidence concerns the gene NFKB1 and viral infectious disease.