Widespread early detection with prostate-specific antigen (PSA) has radically transformed the clinical management of prostate cancer. PSA has become valuable in the monitoring and risk stratification of recurrent disease following local therapy. In many ways, biochemical recurrence-free survival, or PSA outcome, has become a surrogate measure of treatment efficacy following primary local therapy. Given the inherent differences in PSA kinetics following these treatment approaches, the definition of biochemical success or failure is not uniform among therapies. An appreciation of the inherent strengths, limitations, and biases of the standard definitions of failure can provide a more meaningful context within which to interpret the reported outcomes of different treatment modalities.