Indeed, GM-CSF enhances the bactericidal activity of anti-TB drugs in both mouse models and in humans.29–31 However, the observed synergy of GM-CSF is relatively limited due to its side effects, short half-life of ~7 h, and reduced penetration into the lungs.32 Therefore, an alternative strategy is required to improve the bioavailability of GM-CSF in the lungs, which are the primary site of TB. The gene discussed is CSF2; the disease is tuberculosis.