In GC, between 25% and 65% of tumors express PD-L1, and multiple mechanisms have been associated with PD-L1 upregu-lation, including PDL1 gene amplification, structural variations in the 3’UTR of PDL1, polymorphisms in PDL1 promoter, activation of oncogenic PI3K signaling, and cytokine- and chemokine-mediated regulation.47,48 PD-L1 expression in GC has been associated with high density of tumor-infiltrating lymphocytes, with MSI, and with EBV infection.49,50. This evidence concerns the gene PIK3CA and gastric cancer.