Upon infection, these epithelia often sense pathogen-associated molecular pat- terns (PAMPs), such as “non-self” bacterial DNA or viral RNA, which activate pattern recognition receptors and downstream interferon response transcription factors (IRFs) to promote induction and secretion of type-I and -III interferons (IFNs).2,3 Upon IFN engagement, receptor Janus tyrosine kinases (JAKs) become activated, phosphorylating transcription factors STAT1/2 and orchestrating the cell-, tissue-, and organismal-level defense that resists and eliminates pathogens and restores homeostasis.4 This evidence concerns the gene IFNA1 and infection.