When challenged with an antigen via toll-like receptor (TLR)7 or 9, they produce type I interferon (IFN)—IFN-alpha (α) or -beta (β)—through the mTOR signaling pathway.12,14,15 It has been suggested that this continuous stimulation of the immune system by IFN production is involved in the development of autoimmunity.8,16,17 However, the role of pDCs in the AIH pathogenesis is not completely clear. Here, IFNA1 is linked to autoimmune hepatitis.