In some tumours, WNT-driven β-catenin activation in combination with PTEN deficiency mediates metastatic castration-resistant prostate cancer (CRPC).9,10 Similarly, aberrant cellular signalling associated with combined PTEN and Sprouty2 (SPRY2) inactivation can drive aggressive, treatment-resistant prostate cancer.11 Together, these genetic alterations represent a significant portion of prostate tumours. The gene discussed is PTEN; the disease is neoplasm.