KLF5 expression paralleled the severity of gastric preneoplastic lesions (Figure 8A), such that there was a progressive increase in cytoplasmic (Figure 8B) and nuclear (Figure 8C) KLF5 immunostaining in foci of gastritis, intestinal metaplasia (IM), and dysplasia compared to normal gastric mucosa, and these increases were markedly augmented in patients with dysplasia. This evidence concerns the gene KLF5 and dysplasia.