However, in the mouse, it has been shown that loss of p18Ink4c and p16Ink4a can cooperate to induce pituitary tumor formation (Ramsey et al., 2007), suggesting that p18Ink4c may have independent tumor suppressive activity in a pathway parallel to that of its related family member p16Ink4a. The gene discussed is CDKN2A; the disease is neoplasm.