Another study revealed that ESAT-6 induced the proinflammatory M1 phenotype with secretion of IL-6, IL-12, and TNF-ɑ and the induction of an M1 transcriptional signature in human monocyte-derived macrophages at the primary infection of Mtb, and then promoted the switch of M1 macrophages to anti-inflammatory M2 phenotypes at a late stage of the infection, helping Mtb to keep a persistent infection [27]. This evidence concerns the gene IL6 and infection.