PBC destruction mechanisms in DM1 have not been completely clarified; however, a great importance has been attributed to the following mechanisms [13]: (1) expression of the apoptosis stimulating fragment (Fas) and its ligand Fas-L on the surface of CD8+ T-activated cells and PBC, respectively; (2) secretion of proinflammatory cytokines such as IL-1β, TNF-α, and IFN-γ by the different immune cells infiltrated in the islets of Langerhans; (3) production of reactive oxygen species (ROS) such as nitric oxide (NO) by macrophages, DCs, and PBC. The gene discussed is IL1B; the disease is primary biliary cholangitis.