These metabolic changes may play a role in the mechanism of the deactivated phenotype since metabolism and macrophage function are highly dependent.36 For instance, it has been shown that T2D promotes an impaired control of M. tuberculosis in human foamy macrophages by inducing lysosomal dysfunction.37 Additionally, previous work has shown that PMs from Ldlr−/− mice fed a Western diet show a deactivated phenotype.23 38 These macrophages differentiate in a cholesterol-rich and atherosclerotic environment and will become lipid-laden foam cells. The gene discussed is LDLR; the disease is type 2 diabetes mellitus.