There has been a longstanding belief that raising serum testosterone (T) causes rapid growth of benign and malignant prostate tissue, and for this reason concerns about the prostate have figured prominently in discussions regarding the risk-benefit ratio of T therapy (TTh). However, current evidence contradicts this belief. The origin of the belief came from the work of Charles Huggins, who in 1941 demonstrated that castration caused regression of prostate cancer (PCa) in men with metastatic disease, and androgen deprivation therapy remains the mainstay of treatment of men with advanced PCa to this day. Castration has been shown to also cause reduced volume of enlarged prostates in dogs and humans. It has been assumed that since lowering T causes prostate regression, then raising T must cause prostate growth. The error in this thinking is demonstrated by the fact that while prostate tissue has an absolute need for androgens to grow, this need is satisfied at a low serum T concentration, approximately 250 ng/dl. This is called saturation. Raising T beyond the saturation point results in no additional growth. Numerous studies including several large RCTs have now confirmed that TTh does not increase the risk of voiding symptoms from TTh versus placebo due to an enlarged prostate, nor does it increase the risk of developing PCa. Guidelines now allow the use of TTh in men following radical prostatectomy with favorable pathology, and in clinical practice TTh is now being used by many centers in men on active surveillance.