Despite the association outlined above, the effect of PI3K activation on prostate cancer growth pre-clinically is not dichotomous as some cell lines with PTEN loss (e.g., LNCaP) retain sensitivity to castration, while the robust response to castration in de novo disease suggests that most PTEN null tumors retain some sensitivity to androgen deprivation. The gene discussed is PIK3CD; the disease is prostate carcinoma.