IFN‐α expression levels are higher among TB patients than uninfected individuals. In‐vitro IFN‐α does not restrict MTB replication intracellularly. IFN‐γ is associated with anti‐mycobacterial activity. IFN‐α compromised the activity of IFN‐γ. IFN‐α inhibited IL‐1β production and induced the production of IL‐10, which further reduced IL‐1β. IFN‐α enhances IFN‐γ production. IFN‐α and IFN‐γ might be associated with MTB immune escape and disease progression. This evidence concerns the gene IL10 and tuberculosis.