Interestingly, some bacteria seem capable of modulating PPARγ to assist their pathogenesis by manipulating its function in lipid metabolism: mycobacteria, such as those associated with tuberculosis and leprosy, use the hosts' lipids for intracellular survival and replication [1]. Mycobacterium bovis bacillus Calmette-Guérin (BCG) infection induces PPARγ expression and its nuclear localization in human monocytes and enhances lipid body formation in the activated macrophages. The gene discussed is PPARG; the disease is leprosy.