Recently, Mayer Barber et al. showed that the plasma level of interleukin (IL)-1ß, type I IFN (IFN-I) and prostaglandin (PG)-E2—among several other inflammatory mediators—characterized the clinical presentation (severe vs. mild) of Mtb infections in TB patients (7), suggesting that a fine-tune regulation of innate immune response is crucial for TB outcomes. The gene discussed is IL1B; the disease is tuberculosis.