Vitiligo is a skin disease that affects all ethnicities and genders and is characterized by the loss of pigment essentially due to the selective loss of melanocytes. Although it is generally considered a systemic disease associated with polymorphisms in genes involved in the immune response, vitiligo is also considered an oxidative imbalance-associated disease. It represents a multifactorial pathology in which some genetic predisposition and epigenetic factors coupled with some critical biochemical and molecular pathways could play a pivotal role. The aim of this work was thus to review some of the fine cellular mechanisms involved in the etiopathogenesis of vitiligo, mainly focusing on the nonimmunological ones, extensively highlighted elsewhere. We took into consideration, in addition to oxidative stress, both the cause and the hallmark of the pathology, some less investigated aspects such as the role of epigenetic factors, e.g., microRNAs, of receptors of catecholamines, and the more recently recognized role of the mitochondria. Sex differences associated with vitiligo have also been investigated starting from sex hormones and the receptors through which they exert their influence. From literature analysis, a picture seems to emerge in which vitiligo can be considered not just a melanocyte-affecting disease but a systemic pathology that compromises the homeostasis of a complex tissue such as the skin, in which different cell types reside playing multifaceted physiological roles for the entire organism. The exact sequence of cellular and subcellular events associated with vitiligo is still a matter of debate. However, the knowledge of the individual biological factors implicated in vitiligo could help physicians to highlight useful innovative markers of progression and provide, in the long run, new targets for more tailored treatments based on individual manifestations of the disease.