In summary, the referenced chronic corneal sensory-terminal Piezo2 channelopathy could result in the observed broken and dysfunctional regeneration activity in association with the theorized activated transcription, impaired Piezo2–Piezo1 crosstalk, activated LCs, activated corneal keratinocytes and breaks in the wound-healing process, not to mention a Th17/Treg imbalance in the neuroinflammatory link. This evidence concerns the gene PIEZO2 and channelopathy.