Upregulated in ADCs were glandular markers such as mucins MUC3A and MUC13; claudins (which modulate tight junction permeability) CLDN2 and CLDN18, which has recently been targeted therapeutically in advanced gastric and gastroesophageal junction adenocarcinomas [18]; drivers of cell differentiation such as GATA6; hepatic nuclear factors such as HNF1B, FOXA2, FOXA3; and SPINK1 (serine protease inhibitor Kazal-type 1), which has been associated with a number of gastrointestinal and genitourinary cancers [19]. This evidence concerns the gene CLDN2 and gastroesophageal junction adenocarcinoma.