Endometriosis is among the most common gynecological disorders, affecting an estimated 10% of women of reproductive age. In clinical practice, it primarily manifests as chronic pelvic pain and infertility, significantly impairing patients’ daily functioning. Its pathophysiology is complex and involves both local and systemic processes. The mechanisms underlying pain in endometriosis are multifaceted and not limited solely to the presence of ectopic lesions. Both peripheral sensitization and alterations within the central nervous system play a crucial role, often accompanied by neurogenic inflammation and the development of new blood vessels and nerve fibers. Increasing attention is being paid to immunological mechanisms, particularly the role of macrophages with high phenotypic plasticity, which contribute to the persistence of chronic inflammation and support the growth and invasion of endometriotic cells. Endometriosis exhibits numerous features in common with neoplastic processes, including the ability to proliferate under hypoxic conditions, invasiveness, and the induction of angiogenesis and neurogenesis. A better understanding of these mechanisms may, in the future, enable the development of therapies targeting the underlying causes of the disease rather than merely alleviating its symptoms.