Paradoxically, however, the main phenotypes of p27 null mice, namely, increased body size, organ hyperplasia, pituitary tumors, and retinal dysplasia (Fero et al., 1996; Kiyokawa et al., 1996; Nakayama et al., 1996), are not rescued by concomitant deletion of Cdk2, thus suggesting that these p27 null phenotypes are not primarily caused by uncontrolled CDK2 activity (Aleem et al., 2005; Martín et al., 2005). This evidence concerns the gene CDK2 and pituitary tumor.