These promoter constructs were transfected into the Alexander human hepatoma cells which were then treated as shown in Fig. 4D. In terms of the IL-6 response of the CRP promoter, STAT site mutation 3 reduced the promoter activity while mutations in sites 1, 2, and 4 increased activity compared to the wild-type promoter; induction in the promoter activity observed was more in site 1 and 2 mutant constructs as compared to site 4 mutation (Fig. 4D). The gene discussed is SOAT1; the disease is hepatocellular carcinoma.