Rosacea is a common, chronic inflammatory disorder of the facial skin. Although the exact pathogenesis of rosacea is unknown, dysregulation of the innate immune system, neurovascular dysregulation and overgrowth of commensal skin organisms are thought to be involved in the pathophysiology of rosacea. Recently, endoplasmic reticulum stress signaling has become a central mechanism in rosacea pathogenesis. In this review, we briefly summarize the current topics in rosacea pathogenesis, focusing on endoplasmic reticulum stress signaling and the lipid mediator sphingosine-1-phosphate.