It has been shown that recruitment of macrophages is CCL2 dependent, and in CCL2-deficient mice, the migration and transformation of circulatory monocytes into the lung’s IMs is abolished with concomitant loss of Mtb infection control (59). The results were divergent from the earlier reports in the zebrafish infection model of M. marinum, where the Mtb lipid PGL exploits the host CCL2–CCR2 axis to recruit permissive macrophages which serve as a niche for Mtb growth (120, 123). The gene discussed is CCL2; the disease is infection.