The article discusses how *Mycobacterium tuberculosis* (Mtb) persists in the human body by utilizing host cholesterol as a carbon and energy source. The study identifies the *mce4* gene cluster as encoding a cholesterol import system that enables Mtb to derive nutrients from host membranes. While cholesterol import is not essential for initial infection or growth in resting macrophages, it is crucial for long-term persistence in the lungs and for growth in IFN-γ-activated macrophages, which are prevalent during chronic infection. This finding suggests that IFN-γ may sequester pathogens in a nutrient-poor environment, and Mtb's ability to catabolize cholesterol allows it to survive and persist. Mtb is an intracellular pathogen that resides within phagosome-like compartments of macrophages. Early in infection, it replicates rapidly in resting macrophages, but as the immune system becomes active, macrophages are stimulated by T cell-derived cytokines, such as IFN-γ, to produce antibacterial effectors. Although this response controls Mtb replication, the bacteria are able to resist eradication, leading to chronic tuberculosis. The study shows that Mtb can degrade cholesterol and use it as a carbon source, with the Mce4 transporter playing a critical role in this process. The loss of this function impairs bacterial growth during the chronic phase of infection and in IFN-γ-activated macrophages. The study also reveals that Mtb resides in a cholesterol-rich region of the macrophage, indicating that it has access to this compound. This ability to catabolize cholesterol is a unique trait, as few environmental organisms share this capability. Mtb likely inherited this trait from its saprophytic ancestors, allowing it to acquire carbon and energy in an intracellular compartment that is otherwise nutrient-poor. The ability to utilize cholesterol is a major strategy for Mtb to circumvent the host's defense mechanisms, particularly the nutrient restriction caused by IFN-γ activation. The study highlights the importance of cholesterol import for Mtb's survival and persistence in chronic infections.The article discusses how *Mycobacterium tuberculosis* (Mtb) persists in the human body by utilizing host cholesterol as a carbon and energy source. The study identifies the *mce4* gene cluster as encoding a cholesterol import system that enables Mtb to derive nutrients from host membranes. While cholesterol import is not essential for initial infection or growth in resting macrophages, it is crucial for long-term persistence in the lungs and for growth in IFN-γ-activated macrophages, which are prevalent during chronic infection. This finding suggests that IFN-γ may sequester pathogens in a nutrient-poor environment, and Mtb's ability to catabolize cholesterol allows it to survive and persist. Mtb is an intracellular pathogen that resides within phagosome-like compartments of macrophages. Early in infection, it replicates rapidly in resting macrophages, but as the immune system becomes active, macrophages are stimulated by T cell-derived cytokines, such as IFN-γ, to produce antibacterial effectors. Although this response controls Mtb replication, the bacteria are able to resist eradication, leading to chronic tuberculosis. The study shows that Mtb can degrade cholesterol and use it as a carbon source, with the Mce4 transporter playing a critical role in this process. The loss of this function impairs bacterial growth during the chronic phase of infection and in IFN-γ-activated macrophages. The study also reveals that Mtb resides in a cholesterol-rich region of the macrophage, indicating that it has access to this compound. This ability to catabolize cholesterol is a unique trait, as few environmental organisms share this capability. Mtb likely inherited this trait from its saprophytic ancestors, allowing it to acquire carbon and energy in an intracellular compartment that is otherwise nutrient-poor. The ability to utilize cholesterol is a major strategy for Mtb to circumvent the host's defense mechanisms, particularly the nutrient restriction caused by IFN-γ activation. The study highlights the importance of cholesterol import for Mtb's survival and persistence in chronic infections.