The biologic effect of smoking or other inhalants (such as cadmium in pollution [5], asbestos [6], silica [7], textile dust [8], coal [9], or diesel fumes [10]) on RA risk may be due to induction of local pulmonary mucosal inflammation at the bronchioles and alveoli, leading to protein citrullination [11] and the aberrant formation of anti-citrullinated protein antibodies (ACPA) in those with the HLA-DRB1 shared epitope [12–18]. The gene discussed is PRTN3; the disease is rheumatoid arthritis.