Dry eye syndrome (DES) is a prevalent ophthalmic condition adversely affecting up to 80% of the population over the age of 80, with potential debilitating effects on specifi c segments of the population such as contact lens wearers, people who have undergone refractive surgeries, postmenopausal women, and patients suffering from a variety of autoimmune disorders ( 1 ). DES is a multifactorial disease of the tears and ocular surface caused by a deficiency in tear production or excessive evaporation ( 2 ). Regardless of the initiating causes, chronic dryness and the resultant tear fi lm hyperosmolarity leads to infl ammation that jeopardizes the structural and functional integrity of the lacrimal gland, meibomian gland, and corneal and conjunctival epithelial tissues. The gradual destruction of Abstract Meibomian gland dysfunction (MGD) is a leading cause of evaporative dry eye and ocular discomfort characterized by an unstable tear fi lm principally attributed to affl icted delivery of lipids to the ocular surface. Herein, we elucidated longitudinal tear lipid alterations associated with disease alleviation and symptom improvement in a cohort of MGD patients undergoing eyelid-warming treatment for 12 weeks. Remarkably, eyelid-warming resulted in stark reductions in lysophospholipids ( P < 0.001 for lyso-plasmalogen phosphatidylethanolamine, lysophosphatidylcholine, and lysophosphatidylinositol), as well as numerous PUFAcontaining diacylglyceride species in tears, accompanied by signifi cant increases in several PUFA-containing phospholipids. These changes in tear lipidomes suggest that eyelidwarming leads to diminished activity of tear phospholipases that preferentially target PUFA-containing phospholipids. In addition, treatment led to appreciable increases ( P < 0.001) in O -acyl--hydroxy-FAs (OAHFAs), which are lipid amphiphiles critical to the maintenance of tear fi lm stability. Longitudinal changes in the tear lipids aforementioned also signifi cantly ( P < 0.05) correlated with reduced rate of ocular evaporation and improvement in ocular symptoms. The foregoing data thus indicate that excess ocular surface phospholipase activity detrimental to tear fi lm stability could be alleviated by eyelid warming alone without application of steroids and identify tear OAHFAs as suitable markers to monitor treatment response in MGD. -Man Lam, S