Several genetic alterations have been reported as driver event of cancer progression, drug resistance, and relapse, including androgen receptor (AR) variants [57,58], Phosphatase and tensin homolog (PTEN) loss [59,60], and E26 transformation–specific (ETS) gene rearrangement [61,62], among others, as assessed mainly based on tissue samples from tumor entities. The gene discussed is PTEN; the disease is neoplasm.