If they are related to the pharmacological effect of the molecule, these AE are generally both explained by either the effects of TNFα inhibition in physiological immune responses (i.e., infection risk manifested in this RRBR cohort, for example by one case each of lower respiratory tract infection) or by an immune response to the therapeutic protein itself (i.e., hypersensitivity manifested in this RRBR cohort, for example by one case each of anaphylaxis). The gene discussed is TNF; the disease is infection.