Even though some studies demonstrated that persistent or de novo molecular alterations (such as CDKN2A allelic loss and mutations of TP53 or CDKN2A) may be responsible for persistent or recurrent neoplasia, respectively, following endoscopic therapy [21–23], the potential value of these molecular markers is limited because these changes occur early and frequently throughout large areas of BE, before the first histologic sign of dysplasia, or before the emergence of markers of neoplasia or progression as detected by DNA flow cytometry (aneuploidy or elevated 4N fraction) [1–5, 24, 25]. Here, TP53 is linked to dysplasia.