Pathological myopia has traditionally been considered a degenerative disorder caused by mechanical stretching and ischemia of the choroid. However, clinical, molecular, and imaging data show that low-grade chronic inflammation contributes to the onset and progression of myopic retinal degeneration. Studies have identified inflammatory patterns such as multifocal choroiditis/punctate internal choroidopathy (MFC/PIC)-like lesions, periatrophic inflammatory “plumes,” and secondary multiple evanescent white dot syndrome (MEWDS). These changes are often found in places of disruption of Bruch's membrane and retinal pigment epithelium. Laboratory evidence demonstrates cytokine dysregulation, activation of the complement cascade, and involvement of JAK-STAT signaling pathways in the myopic eye. Mechanical stress and hypoxia act as triggers for sustained immune activation that promotes extracellular matrix remodeling, choroidal thinning, and progressive atrophy. Recognition of inflammation as part of the pathophysiology may lead to new therapies, such as immunomodulatory approaches or those targeting complement.