The ability of genetically identical cells to display different phenotypes is a significant obstacle for the treatment of many human diseases. This is especially true for tuberculosis (TB), a bacterial infection caused by Mycobacterium tuberculosis. Heterogeneity plays a key role in TB’s continued presence as a global health threat, providing a huge reservoir of latent disease in the world and preventing cure of active disease. Genetic diversity of either host or pathogen does not, alone, explain all this heterogeneity. We hypothesize that non-genetic sources of heterogeneity in pathogen populations lead to variation in outcome. Testing this hypothesis with conventional methods is difficult as it requires studying pathogen cells as individuals, rather than populations, at timescales that can capture the dynamics of heterogeneity. In addition, developing therapeutics to target heterogeneity demands a deep understanding of the molecular mechanisms underlying this phenomenon. My lab uses a combination of fluorescent reporters, time-lapse microscopy, and bacterial genetics to understand the mechanisms and consequences of phenotypic heterogeneity in mycobacterial populations.