To address the cellular response, Btk-deficient bone marrow-derived macrophages (BMMs) were analyzed at a biochemical and molecular level upon infection with Lm. Btk was activated in BMMs in response to Lm infection and Btk−/− BMMs showed enhanced levels of TNF-α, IL-6 and IL-12p40, while the production of IFN-I remained unaltered. The gene discussed is TNF; the disease is infection.