Overexpression of NF-κB-p65 rescued CCT3-affected cell proliferation and migration in breast cancer cells, as confirmed in an NF-κB-p65 rescue assay.[50] Silencing of CCT3 in cervical cancer cells was detected by bioinformatics analysis, which found that NF-κB-p65 was associated with tumor signaling pathways.[35] Therefore, further exploration of the relationship between CCT3 and the NF-κB signaling pathway may be a feasible research direction for the mechanism of malignant transformation of tumor cells. This evidence concerns the gene CCT3 and neoplasm.