Elevated expression in TB patients of IFN-related genes, TLRs and genes involved in the JAK-STAT signaling pathway (STAT1, OSM and NMI) at first sight seems contradictory to the increased expression of SOCS3, known to inhibit signal transduction emanating from cytokine and TLR stimulation through the JAK-STAT pathway [22], [23]. Here, SOAT1 is linked to tuberculosis.