However, the utility of these molecular markers (including 9p loss of heterozygosity [LOH; site of CDKN2A], 17p LOH [site of TP53], and mutations of TP53 and CDKN2A) is limited, as these changes tend to occur early and frequently, even in non-dysplastic BE, and often before DNA flow cytometric markers of neoplasia or progression (aneuploidy or elevated 4N fraction) are detectable [1–5, 24, 25]. The gene discussed is TP53; the disease is Barrett esophagus.