Rosacea is a common, chronic inflammatory skin disease that affects the central portions of the face, such as forehead, the chin and the lower half of the nose. This graduate thesis will delve into the existing scientific literature that attempts to recognize the pathophysiologic pathways leading to rosacea manifestation. Even though rosacea is one of the most common conditions encountered by dermatologists worldwide, the etiopathogenesis of this inflammatory disease remains somewhat of a mystery. Researches dedicated to epidemiological investigations undeniably point towards a genetic factor; however, no “rosacea gene” has been recognised to date. Although rosacea has a high prevalence among fair-skinned individuals, recent reports show that it can occur in other skin phenotypes as well. While four clinical subtypes have been designated, it is still unknown if the subtypes are a representation of the different developmental stages of the disease or simply manifestations of a syndrome that clinically overlap. This paper classified pathophysiological mechanisms of rosacea as either being the outcome of innate immune dysfunctions, neuroimmune and neurovascular interactions, ultraviolet radiation, and lastly, microbial causation. Many investigative and observational studies have been undertaken in the past few decades to pinpoint the precise pathophysiological pathway, especially clarifying the pivotal role of innate immunity dysfunction in the development of rosacea.