Based on a large amount of collected data, Dallmann-Sauer and authors speculated about the interplay of T cells and alveolar macrophages in TB resisters, proposing that constitutive IFNG expression from T cells combined with alveolar lymphocytosis leads to increased IFN-γ levels, which drive alveolar macrophages toward an M1-like state, priming them for enhanced antimicrobial responses (14, 16). The gene discussed is IFNG; the disease is tuberculosis.