We analyzed the different biological processes and occurrence numbers between low expression inhibited PTHLH downstream-mediated aging gene ontology (GO) network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and the corresponding high expression (fold change ≥2) inhibited GO network of human hepatocellular carcinoma (HCC). Inhibited PTHLH downstream-mediated aging network consisted of aging, branched chain family amino acid biosynthesis, cellular metabolism, cholesterol biosynthesis, coupled to cyclic nucleotide second messenger, cytolysis, 'de novo' GDP-l-fucose biosynthesis, detection of mechanical stimulus, glucose homeostasis, G-protein signaling, leukocyte adhesion, iron-sulfur cluster assembly, JAK-STAT cascade, Notch signaling pathway, nucleotide-sugar metabolism, peptidyl-tyrosine sulfation, protein amino acid N-linked glycosylation, protein amino acid phosphorylation, response to drug, rRNA processing, translational initiation, ubiquitin-dependent protein catabolism, homophilic cell adhesion in no-tumor hepatitis/cirrhotic tissues. We proposed inhibited PTHLH downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network. Our hypothesis was verified by the same inhibited PTHLH downstream-mediated aging GO network in no-tumor hepatitis/cirrhotic tissues with the corresponding activated GO network of HCC, or the different with the corresponding activated GO network of no-tumor hepatitis/cirrhotic tissues. Inhibited PTHLH downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network included TSTA3, ALK, CIAO1, NOTCH3 in no-tumor hepatitis/cirrhotic tissues from the GEO data set using gene regulatory network inference method and our programming.