Initial studies described that both UFL1 and the adaptor protein C53 (CDK5RAP3), reported to function as a tumor suppressor [43,98,99,100], regulates NF-kB signaling by associating directly with RELA (p65), abolishing its phosphorylation to enhance interaction with HDAC thereby stimulating NF-κb activity [47]. The gene discussed is NFKB1; the disease is neoplasm.