On top of that, as these modifications are reversible, the therapeutic interventions using inhibitors of DNA methylation (such as 5-azacytadine) or histone deacetylases (such as romidepsin or entinostat) may result in the re-increase in SLFN11 tumor expression levels and thus re-sensitization to DDA, making SLFN11 an attractive therapeutic target [25,34,42,43,45,46]. This evidence concerns the gene SLFN11 and neoplasm.