CCT6A and neoplasm: The possible reasons were (1) CCT6A promoted cell proliferation and metastasis, which enhanced tumor progression; thus, the CCT6A expression was negatively correlated with DFS and OS in NSCLC patients (as we discussed above) [16, 18]; (2) CCT6A might facilitate drug resistance in NSCLC (as its role in melanoma), which eventually led to unfavorable treatment outcomes; thus, CCT6A high expression predicted worse survival profiles in NSCLC patients [25].