During tumor development, the dominant cellular lineages in monoclonal HDs and EBVaGCs harbored clonal mutations and/or CNAs targeting the PI3K-Akt pathway (PIK3CA/B and PTEN), the Wnt pathway (CTNNB1 and GNAS) [43], and ARID1A (our study, 18/20 patients; TCGA, 24/26 EBVaGC s[5]), whereas these genetic changes were rare in normal tissues and LDs (our study, 5/19 patients) (P = 3.93e−07) (Figs. 2b and 7a). This evidence concerns the gene CTNNB1 and neoplasm.