Benign prostatic hyperplasia (BPH) is a nonmalignant overgrowth of the prostate gland that is associated with lower urinary tract symptoms which deteriorate the patient's quality of life. Despite the high prevalence of BPH among aged men, its pathophysiology is not completely understood. Both androgenic and non-androgenic factors mediate the pathophysiology of prostatic hyperplasia. However, inflammation plays a crucial role in BPH pathophysiology. The inflammatory injury stimulates the production of variant cytokines and local growth factors that induce tissue remodeling and stromal hyperproliferation. Fibroblast growth factors (FGFs) are the most versatile in their ability to regulate cellular proliferation and differentiation. In this review, we will discuss the evidence that supports the role of FGFs in BPH and their signaling pathways involved in stromal hyperplasia.