Schulmann et al., in their retrospective cohort study with 77 EACs, 93 BEs, 20 dysplasias (n = 14 LGD, n = 6 HGD), and 64 NE patients, reported that CDKN2A, RUNX3, and HPP1 inactivation and progression risk increased 2 years before EAC diagnosis in patients with BE [24]. Here, CDKN2A is linked to Barrett esophagus.