In 2011, FcαRI transgenic mice showed protection against tuberculosis after being given a novel human IgA (monomeric IgA1) mAb as part of passive immunotherapy.5 Balu et al. 5 hypothesized that binding of mIgA complexed with M. tuberculosis to FcαRI‐positive alveolar macrophages and/or neutrophils activated antibacterial activity of the infected cells. The gene discussed is CD79A; the disease is tuberculosis.