Furthermore, we recently reported that an individual prone to developing autoAbs generated lifelong neutralizing anti-IFNα autoAbs following IFNα therapy (Fernbach et al., 2024), suggesting that treatment of tolerance-compromised individuals with high doses of IFNβ could also result in the induction of pathogenic anti-IFNβ autoAbs and new long-term infection-susceptibility consequences. The gene discussed is IFNA1; the disease is infection.