• "turn off" certain genes when those particular genes are not needed (e.g., they turn-off genes involved in juvenile development after the organism reaches adulthood).
• prevent the spread/activation of potentially-harmful nucleic acids (e.g., certain transposable elements) within the organism's genome. For example, the mouse pigment gene known as agouti can be rendered defective when a certain transposable element embeds itself in that gene's nearby regulatory sequence; resulting in yellow or mottled mouse fur which is less effective in camouflaging the mouse from predators.

DNA methylation (e.g., of tumor suppressor genes that would normally prevent inappropriate cell division/proliferation) also occurs in some cancers.

Research indicates that some DNA methylations (e.g., accomplished via feeding of a small amount of a methyl group donor compound such as folic acid) can correct certain genetic defects. For example, feeding of folic acid to pregnant mice from a line bearing the above-described defective agouti gene typically results in at least half of her offspring having normal brown color fur.

DEOXYRIBONUCLEIC ACID (DNA),  DNA METHYLTRANSFERASES,  METHYLATED,  CELL,  GENE,  IMPRINTING,  CANCER,  TRANSCRIPTION,  GENETIC CODE,  MESSENGER RNA (mRNA),  P53 GENE,  TUMOR-SUPPRESSOR GENES,  EPIGENETIC,  SHORT INTERFERING RNA (siRNA),  TRANSPOSABLE ELEMENT,  REGULATORY SEQUENCE,  DIFFERENTIATION PATHWAYS,  ALKYLATING AGENTS