Nevertheless, in advanced NSCLCs with positive oncogene mutations such as EGFR and ALK alterations, anti-PD-1/PD-L1 treatment exhibited inferior efficacy than corresponding tyrosine-kinase inhibitors (TKIs) according to the IMMUNOTARGET study [3–5], and the inferior response might be caused by lower PD-L1 expressions, lower tumour mutational burden (TMB), and fewer CD8+ tumour infiltrating lymphocytes and neoantigens in oncogene-positive NSCLCs [6]. This evidence concerns the gene EGFR and neoplasm.