CDKN1B is a gene that codes for a cyclin dependent kinase inhibitor. This protein is an inhibitor of cyclin dependent kinases 2 and 4, and is therefore, involved in arresting the cell cycle at the G1 phase. Specifically, the CDKN1B protein inhibits the cyclin-cyclin dependent protein kinase complexes, especially the Cyclin E-Cdk2, Cyclin A-Cdk2, and Cyclin D-Cdk4 complexes. CDKN1B levels are elevated by cell-cell contact and by elevated levels of cAMP and rapamycin, thereby allowing a mechanism for controlling cellular proliferation. Cellular levels of the protein are also increased after DNA damage. The levels of CDKN1B are themselves controlled by ubiquitin mediated protein degradation. This degradation enables a transition of the cell to the proliferative state

The CDKNIB gene on chromosome 12 (about 500 kb long) shares homology with the CDKN1A gene. The protein, which weighs 22 kDa and consists of 198 amino acids, is homologous to the CDKN1A protein at a 60 amino acid residue segment at the N-terminal end. The C-terminal end contains a nuclear localization signal and a phosphorylation site for ubiquitination. The protein has been found to be expressed ubiquitously in all tissues, although skeletal muscles show a very high level of expression, while relatively lower levels are seen in the liver and kidney.

The gene has also been found to be over-expressed in aggressive B cell lymphomas, while its expression is several different forms of carcinomas. Interestingly, in leukemias and some other cancers with a poor prognosis, the gene has been found to be deleted. In breast cancer, expression of the gene has been linked to severity of the condition, with lower levels of expression significantly associated with disease free survival. Mutations in the gene are also responsible for Multiple Endocrine Neoplasia Type 4, a condition characterized by cancers of the thyroid.