As a central regulatory hub in inflammation‐related tumorigenesis, aberrant activation of NF‐κB mediates enhanced proliferation and inhibition of apoptosis in tumor cells.[28] Experimental evidence suggests that CLTB maintains sustained activation of the NF‐κB signaling pathway by promoting IκBα and p65 phosphorylation modification, thereby upregulating the PCLAF expression level. The gene discussed is NFKBIA; the disease is neoplasm.