For example, loss of p27 on a heterozygous PTEN background leads to a dramatic increase in the incidence of precursor lesions which progress to carcinoma in situ or even invasive carcinomas of the prostate, while PTEN mice with intact p27 expression develop fewer precursor lesions which do not progress to more malignant states [20]. The gene discussed is CDKN1B; the disease is in situ carcinoma.