While PD-1, IL-10, TIGIT, and other immunosuppressive molecules may limit inflammatory pathophysiology associated with TB, they may also inadvertently foster a microenvironment conducive to Mtb persistence,73,74,75 highlighting the importance of balanced interplay between IL-10 and other immunoregulatory molecules and type 1 immunity in anti-TB immunity.76 This evidence concerns the gene PDCD1 and tuberculosis.