Limbal epithelial stem cells (LESCs) play critical roles in regulating homeostasis of the corneal epithelium. Loss of LESCs leads to severe corneal disease, called limbal epithelial stem cell deficiency (LSCD), which is associated with corneal neovascularization, stromal scarring and impaired visual acuity. 1 LESCs transplantation represents a feasible therapeutic approach to LSCD, but according to statistical analysis of clinical trials, this approach has nevertheless failed to improve vision in 26.7%-60% of LSCD patients. These therapeutic failures may be due to the limited life span of LESCs. 2-12 Evidently, a detailed analysis of the molecular mechanisms of LESC maintenance is of paramount importance to design approaches to enhance the success of therapeutic transplantation, or better still, to be able to interfere with LESC loss early in the disease process. 13 The maintenance of adult stem cells relies on stem cell niches whose microenvironment contains an extracellular matrix and cells that provide autocrine and paracrine signals necessary for the proper function of the respective stem cells. There is increasing evidence that one of the major type of niche cells supporting