To explore whether a p27-dependent checkpoint induces senescence upon AKT activation, and that the ablation of this checkpoint, allows the progression from MIN to carcinoma, as has been suggested in prostate models [31], first, we checked whether p27 was activated in benign lesions and/or lost in tumors (adenosquamous or carcinoma) in our myrAKT mice. Here, AKT1 is linked to carcinoma.