Given that monocytes highly express CCR2 and CX3CR1 and that monocyte trafficking to the Mtb-infected lung is not completely abrogated in CCR2-deficient mice, we generated mice deficient in both CCR2 and CX3CR1 and used them to evaluate the accumulation of monocyte-derived cells and Mtb control in the lungs and mediastinal LNs (MLNs) following aerosol infection. The gene discussed is CX3CR1; the disease is infection.