Deoxycytidine analog that incorporates into DNA during replication and covalently traps DNMT1, causing its progressive depletion — a more potent and DNA-selective demethylation mechanism than azacitidine. The SDH-specific rationale rests on direct experimental evidence: Letouzé et al. (Cancer Cell 2013, PMID: 23707781, DOI: 10.1016/j.ccr.2013.04.018) demonstrated that succinate accumulation in SDHB-deficient mouse chromaffin cells established a hypermethylated, pro-migratory epigenetic phenotype driven by TET enzyme inhibition — and that decitabine treatment directly reversed this migratory phenotype in vitro. This makes decitabine the only DNMT inhibitor with cell-model evidence of phenotypic rescue in SDH-deficient cells. CIMP in SDH-deficient GIST further established by Killian et al. (Cancer Discov 2013, PMID: 23550148, DOI: 10.1158/2159-8290.CD-13-0092).