Allergic conjunctivitis (AC) is a common ophthalmic disease, ranging from mild, self-limiting forms to severe, vision-threatening conditions such as vernal keratoconjunctivitis and atopic keratoconjunctivitis. Its pathogenesis originates from the interplay between genetic predisposition and complex environmental factors, manifesting as a complex pathophysiological network. This review comprehensively elucidates recent advancements in the etiology and pathogenesis of AC. Key etiological drivers include Ig(Ig: Immunoglobulin) E-mediated reactions due to allergen sensitization, genetic susceptibility, and escalating environmental impacts, such as climate change, air pollution, and modern lifestyles influencing immune development and allergen exposure. Its pathogenesis is characterized by complex immune cell activation and crosstalk; dysregulation of lipid mediators; an intricate cytokine network predominantly driven by Th2(Th2: T helper 2) cytokines and alarmins that often signal via the JAK-STAT(JAK-STAT: Janus Kinase- Signal Transducer and Activator of Transcription) pathway; and a significant neuroimmune imbalance leading to neurogenic inflammation and persistent itch. Furthermore, epithelial barrier dysfunction, ocular surface microbiome dysbiosis, and epigenetic modifications are increasingly recognized as crucial regulatory factors. This review also highlights the ongoing challenges in addressing AC heterogeneity, pursuing personalized medicine, improving diagnostic methods, and developing effective preventive strategies, including allergen immunotherapy. Ultimately, integrating multidimensional data from cutting-edge research holds the promise of achieving more precise and personalized AC management, thereby improving outcomes for AC patients worldwide.