Most importantly, in childhood TB, the immune inhibitory molecules, IL1RN and IL1R2 which inhibit functional IL1 signaling and molecules involved in generation of an adaptive immune response (CD40LG, HAL-DOB, CD28) that were downregulated is consistent with emerging evidence linking the cross talk between IL1 and type 1 IFN to TB and which provide potential targets for host directed therapy (Mayer-Barber et al., 2014). The gene discussed is HAL; the disease is tuberculosis.