Mycobacterium tuberculosis is a deadly pathogen responsible for millions of deaths worldwide. Treatment for Tuberculosis has been made especially difficult due to the rising prevalence of multidrug resistant strains. Drug resistant strains not only spread from patient to patient, but also emerge spontaneously from susceptible strains. Subpopulations of M. tuberculosis often persist through antibiotic exposure, despite lacking known genetic markers. These “persister cells” survive long enough for the infection to develop full antibiotic resistance. One potential source of this heterogeneous drug response is epigenetic regulation. In many bacterial species, DNA methylation regulates gene expression and causes phase variation. Phase variation maintains heterogeneous phenotypes in an isogenic population, allowing the bacteria to employ multiple survival strategies simultaneously. In uropathogenic Escherichia coli and the pathogen Salmonella enterica, the MTase Dam causes phase variation by interfering with transcription factor binding, blocking the transcription of specific genes when their promoters are methylated. A characteristic signal of this phenomenon is site specific hypomethylation. I searched for this characteristic signal in the sequencing kinetics of 93 clinical M. tuberculosis isolates, and discovered 95 loci of consistent site specific hypomethylation. Most of these sites matched the characterized binding site motifs of known transcription factors in M. tuberculosis, suggesting that they form a similar epigenetic switch to those demonstrated in E. coli and S. enterica. MTase motifs overlapped predicted promoter elements in 85 sites, further supporting their regulatory role. Genes downstream of these methylated promoters were functionally enriched for transmembrane proteins. Variation in the expression of these genes could allow M. tuberculosis to adapt to its environment.