To test the idea that autoimmune hepatitis (AIH type I) in young people is caused by differences in how patients’ and controls’ proinflammatory genes respond to viral triggers. The expression of genes inside the liver was compared between AIH type I patients (n=24, ages 9–30) and controls (n=21, ages 4–25). The complementary DNA (cDNA) libraries made from the total RNA taken from formalin-fixed paraffin-embedded (FFPE) liver biopsy samples were used for RNA sequencing. The levels of gene expression were measured, and the functions of genes that were expressed differently were looked at. The databases Kyoto Encyclopedia of Genes and Genomes (KEGG) and PANTHER were used to look at pathways. The rest of the sequences were matched to the full set of viral genomes in RefSeq. Differential gene analysis found that the expression of 181 genes was significantly different (136 upregulated in the AIH group). Autoimmune pathway genes like CD19 and CD20, which help control and mature B cells, as well as T-cell-related genes like CD8 and LY9, were turned up in our AIH group. Samples from the AIH group had higher levels of CXCL10, which is thought to be linked to the severity and progression of AIH, complement genes (C1QA, C1QB, and C1QC), and human leukocyte antigen (HLA) genes (HLA-DRB1, HLA-DRA, HLA-B, and HLA-C). There were no specific viral causes that were found. Next-generation sequencing and differential gene expression analysis of the AIH group have not only shown that B cells play a role in the cause and treatment of AIH, but they have also shown that CXCL10 (anti-CXCL10) and a few genes related to the complement system could be used as new therapeutic targets.