It could be assumed that susceptibility to the VEGF inhibitor in patients with NSCLC and liver metastases arises from the reversal of immune suppression by the VEGF inhibitor, which basically has reduced-infiltration CD8+ T-cells, which may further enhance the T-cell-mediated killing of cancer cells by the PD-L1 inhibitor [13]. This evidence concerns the gene CD274 and non-small cell lung carcinoma.