The possible reasons for this result might be as follows: as the influence of CCT6A on cellular functions in other cancers, CCT6A might enhance malignant cell proliferation via accelerating the G1-to-S transition, which further facilitated the NSCLC occurrence; thus, increased CCT6A expression was observed in tumor tissue compared with adjacent tissue in NSCLC patients [17, 18]. This evidence concerns the gene CCT6A and cancer.