Overactivated STAT3 can lead to the downregulation of immune-stimulating factors and is often found to interact with NF-κB, facilitating immune evasion by tumor cells.[37] Cui et al[22] experimentally verified that silencing CCT3 reduced the activity of STAT3 in the nucleus of liver cancer cells, even under IL-6 stimulation, indicating that silencing CCT3 negatively regulates the IL-6-STAT3 signaling pathway. The gene discussed is STAT3; the disease is neoplasm.