To determine whether the requirement for CDK4 in menin-associated tumorigenesis is unique among the G1-regulatory CDKs or there is functional overlap, we next examined the impact of Cdk2-deficiency on tumorigenesis of Men1+/− mice, by generating Men1+/−; Cdk2−/− and Men1+/−; Cdk2+/+ (Cdk wild-type) littermates. In sharp contrast to Men1+/−; Cdk4−/− mice, 51% of examined Men1+/−; Cdk2−/− mice (n=29) showed macroscopic pituitary tumors comparable to those in Men1+/−; Cdk wild-type mice (Fig. 1A, 1B). Interestingly, we observed tumors in 4 (24%) of 17 Men1+/−; Cdk2−/− male mice and 11 (92%) of 12 Men1+/−; Cdk2−/− female mice. This may imply that Cdk2 deficiency modestly promoted pituitary tumorigenesis under the conditions of the study, although examinations of a larger cohort will be necessary to be conclusive. Regardless, these data indicate that the absence of CDK2 can be compensated, and has no impact on restraining the process of pituitary tumorigenesis induced by menin deficiency.