Dry eye disease (DED) is a multifactorial disease characterized by a loss of homeostasis of the tear film and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles (Belmonte et al., 2017). Interestingly, DED shares common characteristics with neuropathic pain, which is defined as pain caused by damage or disease affecting the somatosensory nervous system. Ocular pain, more commonly called corneal pain, has gained recognition due to its increasing prevalence, morbidity, and resulting social burden (Belmonte et al., 2017). To date, the management of chronic corneal pain still represents a therapeutic challenge. A better understanding of the molecular and cellular mechanisms participating in the transition from acute to chronic pain are crucial issues for developing the effective management and a therapeutic strategy to alleviate this debilitating condition. Today, much of the knowledge of neuroinflammation-neuropathic pain processing comes from data from the spinal cord, but a comparatively small number of investigations have been carried out in the corneal trigeminal pain pathway.