Interestingly, PBMCs from the non-IRIS patients produced minimal levels of IFN-α, IFN-γ, IP-10 and IL-12, following stimulation, and inhibition of the MyD88 adaptor did not reduce production of other cytokines/chemokines, further suggesting that the dysregulated cytokine/chemokine production via MyD88 signalling contributes to TB-IRIS. The gene discussed is IFNA2; the disease is tuberculosis.