Indeed, a higher multiplicity of infection (Schwann dataset) leads to activation of the type I IFN pathways (OAS1, TRIM7, TNFSF10) and subversion of energetic metabolism where increased glucose uptake is redirected from glycolysis/mitochondrial respiration to lipid metabolism (MVK, DHCR7, HMGCS1, LDLR, MSMO1)  (3, 12). The gene discussed is MSMO1; the disease is infection.