CAVIN3 and neoplasm: PRKCDBP is a proapoptotic tumor suppressor which is commonly altered in CRC by promoter hypermethylation, and its gene transcription is directly activated by NF-κB in response to TNFα, which suggests that PRKCDBP inactivation may contribute to tumor progression by reducing cellular sensitivity to TNFα and other stresses, particularly under chronic inflammatory microenvironment [38].