In addition, dual-luciferase assay indicated that ITLN1 facilitated the HNF4α promoter activity, and ectopic expression or knockdown of NFκB-p65 restored the changes in HNF4α promoter activity induced by stable transfection of ITLN1 or sh-ITLN1 in gastric cancer cells, while these effects were abolished by mutation of NFκB-p65 binding site (Figure 2C). Here, HNF4A is linked to gastric cancer.