In fact, many genetic and chromosomal abnormalities detected in BE (including 9p LOH [site of CDKN2A], 17p LOH [site of TP53], and mutations of TP53 and CDKN2A) tend to occur early and frequently throughout large areas of BE5–10,112–114, even before the first histologic sign of dysplasia, limiting their utility as a diagnostic or prognostic marker of dysplasia in BE patients. Here, TP53 is linked to Barrett esophagus.