Thus, Cdk4R/R/Cdkn1b+/− and Cdk4R/R/Cdkn1b−/− mice, which would be null for p27 and have a mutant of CDK4 that renders it insensitive to INK4 inhibitors, have been reported to develop pituitary tumours with complete penetrance and a short latency, thereby indicating that there is co-operativity between p27 and CDK4 (Sotillo et al., 2005). The gene discussed is CDK4; the disease is pituitary tumor.