Though the exact causation of vitiligo still eludes us, it is safe to assume that several different pathophysiologic mechanisms may be involved. Best supported is the autoimmune hypothesis because of the numerous genetic associations and linkage studies, in combination with abnormal cellular and humoral immunity. However, the exact contribution of the aberrant immune responses in vitiligo pathogenesis has not yet been permanently established. The neural, humoral, cytotoxic, and oxidative stress hypotheses have modest evidence. The concept of melanocytorrhagy and decreased melanocyte survival still has to be convincingly demonstrated. Because all these ideas show promise, it seems probable that vitiligo, in reality, may be a final end result of a variety of anomalies that exhibit a common phenotype. The triggers underlying vitiligo pathogenesis may vary depending on the type and distribution of vitiligo patches. Further research works are necessary to clarify the interaction of all the abovementioned mechanisms and factors for a better comprehension of the pathophysiology of vitiligo and subsequent successful management.