Abstract
Cancer arises from a convergence of genetic mutations and epigenetic alterations. Among the consequences of epigenetic deregulation is the aberrant activation of transposable elements, particularly retrotransposons, the most expansive and functionally impactful class. This review examines the paradoxical role of retrotransposons in cancer, emphasizing their dual capacity to support oncogenesis while simultaneously triggering innate and adaptive immune responses that may limit tumor growth. A central question is discussed: Is retrotransposon activation merely a stochastic byproduct of epigenetic instability, or could it represent an intrinsic layer of early tumor surveillance that inadvertently turns against the host as malignancy progresses?