Tumour mutation burden, tumour immunosuppressive microenvironment, and PD-L1 expression are strongly associated with the response to immune-checkpoint inhibitors.7,8 In addition, the advantages of these inhibitors in improving prognostic outcomes in STAD has been shown to vary with different patient ethnicities, different immune-checkpoint inhibitor categories, microsatellite instability, and tumour mutational burden.9 Furthermore, many genetic biomarkers currently ignore clinical pathological features and do not reflect the immune status of patients. This evidence concerns the gene CD274 and neoplasm.