Indeed, they demonstrated that monocytes differentiated towards M2-like macrophages (CD16+CD163+MerTK+) depending on the IL-10/STAT3 signaling pathway in the context of TB, and that this phenotype rendered the host permissive to intracellular M. tb growth and an impaired ability to activate the Th1 immune response [12]. Here, STAT3 is linked to tuberculosis.