this study are sensory in origin and may share common propensity, , that alcohol targeted the programmed DNA methylation of many sensory receptors. Our previous study in embryo development also revealed that the DNA methylation of a large number of (>100) olfactory genes was altered by alcohol exposure in a similar dose (Liu et al., 2009). These two studies point to a general effect of alcohol on DNA methylation in sensory reception genes, particularly olfaction. It is interesting that the findings also indicated that after prenatal alcohol exposure, a major defect was found in olfactory bulb development (Kirstein et al., 1997, Maier and West, 2001, Abate et al., 2002). The major alteration of the DNA methylation program may provide a mechanism for such neurodevelopmental deficit (e.g. sensory deficits) in FASD. Although the consequence of the methylation on DRG gene expression is yet to be verified, the function of the DNA methylation change was demonstrated by us and others by treating NSCs with 5-azacytidine (5-AZA), which inhibits DNA methyl transferase, and the new DNA-methylation at the time of differentiation (Matsuda, 1990, Singh et al., 2009b). Retardation of migration, process growth, and key neural phenotype expression were evident. The necessity of methylation
