Epigenetic information can be transmitted from one generation to the next in a phenomenon referred to as transgenerational epigenetic inheritance (TEI), where gene expression patterns are inherited with no change to the DNA sequence. This has been observed in a variety of species, including Mus musculus, Drosophila melanogaster, and Caenorhabditis elegans and has implications for natural selection, viral defence, and germline immortality. Here, we utilize C. elegans in an RNA interference (RNAi) assay where parent animals are exposed to an RNAi trigger to silence a gfp transgene and subsequent generations are assessed for gfp expression in the absence of this trigger. Previous work has distinguished three distinct parts to this transgenerational silencing process, including initiation of gene silencing, the establishment of silencing inheritance within the parental germline, and the maintenance of this silencing signal within the progeny. The highly identical predicted histone methyltransferases set-9 and set-26 as well as a third similar gene termed Y73B3A.1 were examined using this assay. We showed that all three are involved in the establishment of a heritable silencing signal and that set-26 is also needed to maintain this signal through multiple successive generations. Both set-9 and set-26 are predicted to have a PHD finger and a SET domain. By mutating key residues within these predicted domains, we determined that they are required for each gene’s function in TEI. Furthermore, a modified version of the aforementioned RNAi inheritance assay, revealed that both set-9 and Y73B3A.1 are likely needed within the parent animals in order to properly establish a heritable silencing signal. Taken together, our findings show that, although these three genes are highly homologous, they each impact TEI in different ways.