Enrichment of PIK3CA mutations in the EBV subtype has been well established within TCGA‐GCC.5 Not surprisingly, the upregulated PIK3CA SMGs in the TCGA‐GCC tumors are highly enriched in M102 (Bonferroni FET p = 1.89E‐110, 14.3 FE), and M102 key drivers including TIGIT (co‐inhibitory Ig receptor) show higher expressions in EBV subtype, compared to other subtypes (Fig. 4b). This evidence concerns the gene PIK3CA and goblet cell carcinoma.