During the progression of esophageal cancer initiated by chronic inflammation, vimentin+ α-SMA+ myofibroblasts migrate to sites of intestinal metaplasia and dysplasia, and may become an innocent bystander in tumor progression by directly enhancing proliferation of nearby epithelial cells in an NF-κB-dependent manner as well as indirectly by recruiting and polarizing cells of the adaptive and innate immune system toward a tumor-promoting phenotype [140]. Here, NFKB1 is linked to neoplasm.