CDKN2A and neoplasm: Genomic profiling has confirmed the status of the main EAC drivers reported in the literature (e.g., TP53, CDKN2A, and PIK3CA) (Secrier et al., 2016a; Cancer Genome Atlas Research et al., 2017; Frankell et al., 2019) in EAC organoids, and mutations and copy-number alterations are consistent with patient-matched tumours.