In an NF-κB-p65 rescue experiment, the overexpression of NF-κB-p65 was shown to rescue cell proliferation and migration in breast cancer cells affected by CCT3 knockdown.[50] In cervical cancer cells, silencing CCT3 through bioinformatics analysis revealed that NF-κB-p65 is associated with tumor signaling pathways.[35] Thus, further exploration of the relationship between CCT3 and the NF-κB signaling pathway may provide a viable research direction for understanding the mechanisms of tumor cell malignant transformation. The gene discussed is NFKB1; the disease is neoplasm.