<p>DNA methylation constitutes a key epigenetic modification that is essential for the regulation of gene expression, the maintenance of genomic integrity, and the establishment of cellular identity and lineage. Aberrations in the regulatory mechanisms controlling DNA methylation have been implicated in the pathogenesis of numerous diseases, most notably cancer. In malignant cells, DNA methylation landscapes are characteristically altered, exhibiting widespread hypomethylation across the genome coupled with site-specific hypermethylation, particularly within CpG islands located in gene regulatory regions. Early investigations identified Tumor Suppressor Genes (TSGs) as primary targets of such hypermethylation, thereby supporting a prevailing model in which epigenetic silencing of TSGs contributes to oncogenesis. However, recent advances in large-scale genomic and epigenomic profiling have revealed a more complex landscape, suggesting that the classical model may be insufficient to fully explain the role of DNA methylation in cancer development. This review aims to elucidate the molecular mechanisms underpinning aberrant DNA methylation in cancer and to critically evaluate its potential as a target for therapeutic intervention.</p>