Various congenital anomalies of the eyelids can result from abnormal tissue proliferation, fusion, and reopening of the eyelids. Therefore, it is important to study the molecular mechanisms underlying eyelid development, focusing on cell behaviors. Mammalian eyelid development occurs in four steps: specification, growth, epithelial fusion, and reopening. Epithelial-mesenchymal interactions are fundamental processes during eyelid formation, and epithelial factors functioning within the eyelid epithelium are also critical. Studies with mutant and genetically modified mice have revealed that various signaling pathways and transcriptional factors are involved in mouse eyelid development. In this review, eyelid morphogenetic factors or pathways are described, as revealed by their mutant phenotype, eye-open at birth (EOB). These include FGFR2b-FGF10, EGFR-ERK, MEKK-JNK, BMP, Shh, Wnt, GPR48, Jun, Forkhead, and Grainyhead.