Strikingly, joint alterations in two or more of RB1, TP53 and/or PTEN were shown to correlate with this aggressive clinical phenotype similarly to SCPC, consistent with preclinical models that support the role of combined tumor suppressor alterations in prostate cancer progression and development of resistance to novel hormonal agents [15,43,44,51]. The gene discussed is PTEN; the disease is prostate cancer.