Previous studies have found increased levels of fascin in dysplastic epithelia (26) or fascin levels increasing gradually in the progression from normal epithelia to simple hyperplasia, dysplasia, carcinoma in situ, to invasive esophageal SCC (26), supporting the assumption that unexpected observation of fascin expression in normal epithelia may reflect pre-malignant changes at the molecular level. This evidence concerns the gene FSCN1 and in situ carcinoma.