Mice and macrophages lacking cathepsin B activity showed obvious resistance to the cytosolic pathogen Francisella novicida CTSB-knockout animals produced fewer pro-inflammatory cytokines and chemokines in the liver.[19] Moreover, F. novicida exploited the activity of CTSB, resulting in permissiveness to bacterial replication and increasing susceptibility to infection. The gene discussed is CTSB; the disease is infection.