Both GBP5 and DUSP3 are involved in the pro-inflammatory response and are upregulated in TB: inducible GBP5 has been shown to mediate the antiviral interferon response during influenza A virus infection [6] and human immunodeficiency virus type 1 (HIV-1) [7], although DUSP3 plays a nonredundant role as a regulator of innate immune responses by mechanisms involving the control of ERK1/2 activation, tumor necrosis factor (TNF) secretion, and macrophage polarization [8]. Here, DUSP3 is linked to tuberculosis.