The rationale for its use as the primary clinical biomarker is based on the premise that EAC in BE patients develops through a sequence of molecular (i.e., loss of CDKN2A followed by TP53 inactivation and aneuploidy) and morphologic changes that begin with intestinal metaplasia and then progress from LGD to HGD, and ultimately to EAC3,5,68,71,78–82. Here, CDKN2A is linked to Barrett esophagus.