TP53 and esophageal adenocarcinoma: One model proposed by Maley and coworkers suggests that an initial mutation (most commonly inactivation of p16) confers a selective advantage to a cell population and this mutation is present in most of cells of Barrett’s esophagus; the acquisition of additional mutations (i.e., inactivating TP53 mutations) give rise to cell clones able to expand across the Barrett’s lesion [22].