Epigenetic marks alter the expression and function of DNA through mechanisms such as DNA methylation, histone modifications or RNA induced silencing. Some of these marks are inherited between generations, influencing gene expression in offspring. DNA methylation was previously considered to be absent in C. elegans as they lack canonical 5-methylcytosine (5mC). Recently however, N6-methyldeoxyadenine (N6mA) has been identified as a rare type of DNA methylation thought to present, at low levels, within C. elegans. The prevalence of N6mA is controversial as its low abundance makes reliable sequencing detection quite difficult and so multiple independent techniques must be used to validate all findings. We have found that the N6mA demethylase NMAD-1 is required for the establishment of a transgenerational silencing signal and preliminary data indicates that N6mA likely interacts with histone methylation to regulate inherited gene expression. NMAD-1 mutants also display increased RNAi sensitivity indicating that this N6mA mark may play a role in regulating RNAi machinery. We have used nanopore sequencing investigate the changes in N6mA levels between generations after the silencing trigger. We have a developed a NMAD-1 catalytic mutant, with no demethylase activity, to confirm whether the transgenerational role of this protein is dependent on its ability to modify N6mA. And also developed a double mutant of NMAD-1 and DAMT-1, the adenine methyltransferase, to examine whether a lack of N6mA can abolish the NMAD-1 heritable silencing defect.