This collection enlarges the sequence specificities of DNA targets and raises the possibility that environmentally-induced bacteria/ phage/plasmid methylases might modify the aphid host genome. In conclusion, for each scaffold we have examined the location of methyl group densities present in promoters and/or in gene bodies and the variation of transcription in the vicinity of these methylations. Many methylated loci associated to enhancers likely regulate gene expression from a long distance in the linear sequence but act closely to the promoters by chromosome folding. These dynamic complex interactions make the correlation methylated DNA/gene expression very difficult to apprehend. Actual methodologies are still primitive to advance in this topic. However, we observed that methylation inversely correlates with gene expression for some analyzed metabolic pathways and seems to proceed in opposite ways for others. Moreover, if a correlation can be demonstrated in many cases, it seems absent for others. This suggests strongly that covalent modification of DNA induced by the environment might have a broad effect on genes by global modification of euchromatin/heterochromatin structure in chromosomes. However, this work allowed us to group the genes that vary between the two analyzed environments in categories of molecular functions or biological processes. Specific metabolic pathways highlighted by GO analysis are consistent with 1,9-Dideoxyforskolin environmental adaptability. We hypothesize that epigenetic stable marks might be transmitted through generations in clonality context and that the sexual barrier in fall could preserve those that are advantageous for the wave of clonal individuals the next spring. By this work, tools like the full differential transcriptome and the full methylome databases between 7-Chlorokynurenic acid environment-selected variants issued from a single founder mother might help to investigate the gene network re-organization in a fluctuating environment. The treatment of older patients with acute myeloid leukemia still poses a substantial therapeutic challenge. Recently, the DNA hypomethylating agent decitabine was approved for this indication based on its significant single agent activity with a very favorable safety profile in large phase II and phase III clinical trials,. Nonetheless, almost half of the AML patients receiving this drug do not show a response, prompting investigations of combination therapy with pan- or class-I specific HDAC inhibitors, or biologicals such as retinoids. Retinoic acids modulate complex physiological events, which trigger key steps during cellular proliferation, differentiation and apoptosis in normal and malignant cells. The beneficial effects of retinoid-based ����differentiation therapy���� have been clearly demonstrated in acute promyelocytic leukemia : the combination of anthracycline-based chemotherapy or arsenic trioxide with all-trans retinoic acid resulted in almost complete cure rates of one of the previously most fatal subtypes of acute myeloid leukemia,.