The possible reasons could be that (1) the binding between a PD-1 inhibitor and PD-L1 could promote antitumor immunity and inhibit immune escape, which may suppress CRC tumor growth (27); (2) apatinib may synergize the antitumor effects of a PD-1 inhibitor (28), thus indicating that PD-1 plus apatinib had potentially better treatment efficacy than apatinib monotherapy; and (3) the sample size of this study was relatively small, which resulted in low statistical power, which indicated no statistical significance was observed in the treatment response between groups. The gene discussed is PDCD1; the disease is neoplasm.