<p>Smut disease in sugarcane, caused by the biotrophic fungus <i>S. scitamineum,</i> is a major challenge in global sugarcane cultivation. The pathogen is airborne and sett-borne, and the fungus establishes in the meristematic tissue of sugarcane plants, leading to the development of whiplike structures as the characteristic symptoms. The teliospores produced in smutted whips are capable of initiating infection in a susceptible host. As a peculiar characteristic of smut fungi, teliospores germinate to produce sporidia, and infection depends on the mating of bipolar sporidia to establish the dikaryotic hyphae that cause the disease. The pathophysiological studies have revealed the alteration in carbon partitioning and energy production, shifting sucrose storage to smut sorus development. The notable auxin mobilization and hormonal imbalances have been reported in infected plants during whip emergence, which denotes the transcriptional reprogramming during infection. Moreover, the overexpression of lignin and invertase biosynthetic genes has been correlated with the proliferative phase of the pathogen in a susceptible host. The studies on host–pathogen interaction revealed the involvement of fungal pathogens effectors, which mimic plant signaling peptides to weaken the immunity and promote disease development. The hot and humid weather and other parameters (wind, light intensity, soil type) contribute to disease initiation and spread based on the prevalence of susceptible hosts in the fields. This review provides a mechanistic insight into epidemiology, infection mechanisms, infection-induced alterations in host physiology and effector biology of <i>S. scitamineum</i> in sugarcane.</p>