It has been postulated that the TMPRSS2-ERG fusion, which has been identified in about 50% of prostate tumors,61 has a role in androgen-dependent tumor growth.62 There is evidence to suggest a relationship between TMPRSS2-ERG status and degree of PSA decline in chemotherapy-naïve patients treated with abiraterone, thereby suggesting a possible role as a putative biomarker for abiraterone response.63 The authors reported that 12 of 15 (80%) patients with an ERG rearrangement had a PSA decline of at least 90%, whereas only 20 of 62 (32.2%) lacking this rearrangement had such a PSA decline. The gene discussed is KLK3; the disease is neoplasm.