Although we found evidence of increased apoptosis within our experimental animals treated either at 2 wks or 6 wks of age (Figure 6), mice injected at 2 wks still progressed to PINs and microinvasive cancer more rapidly suggesting that the delayed latencies seen following Pten excision at 6 wks of age might have been a consequence of tumorigenic changes being targeted to a residual population of cells that had evaded the Pten loss-induced senescence response. The gene discussed is PTEN; the disease is cancer.