Conversely, high HBsAg load may drive the development of anti-IFNα auto-Abs, due to the potential induction of IFNα during spontaneous hepatic flares32 There is minimal structural homology between T1 and T3IFNs, which suggests that the presence of auto-Abs against multiple IFN subtypes, rather than evidence of cross-reactivity, represents broad breaches of immune tolerance as seen in COVID-19. The gene discussed is IFNA2; the disease is COVID-19.