Pathogenesis of vitiligo is complex and involves interplay between inherent susceptibility of melanocytes to stress, external and internal factors leading to oxidative stress and immune dysfunction. Various theories have been proposed with scientific evidence supporting each one of them. Role of genetics and inherited genetic susceptibility loci in the pathogenesis has been proven. Neural theory implicates neuromediators and catecholamines, while biochemical theory blames melanogenesis byproducts and other biochemicals in damaging melanocytes. According to the oxidative stress theory, which is one of the widely accepted theories, it is the internal imbalance between reactive oxygen species and antioxidants, along with mitochondrial dysfunction which leads to melanocyte death. As per melanocytorrhagy theory, deficiency of cell adhesion molecules leads to detachment of melanocytes from basal layers and their loss. Whereas intrinsic death theory proposes activation of apoptotic cascade due to internal defects in melanocytes as the melanocyte death mechanism. Immune theory describes the role of both adaptive and innate immunity and activation of immune system to be ultimately responsible for disease progression and continuation. Stem cell theory hypothesizes decreased capacity of stem cells to regenerate lost melanocytes to be the basis of depigmentation. A flowchart summarizing and interconnecting all the possible pathways of pathogenesis has also been depicted. The role of histopathology in the diagnosis of vitiligo is not yet fully established. The diagnosis is made primarily on clinical grounds. Biopsy is usually done in difficult cases to rule out the differential diagnoses.