The inheritance of genetic information has long been established and it is now apparent that epigenetic information can also be transmitted from one generation to the next. This phenomenon, where gene expression patterns are inherited with no change to the DNA sequence, is referred to as transgenerational epigenetic inheritance (TEI). It has been observed in a range of species, including Mus musculus, Drosophila melanogaster, and Caenorhabditis elegans and has implications for natural selection, viral defence, and germline immortality. The research presented here utilizes C. elegans in an RNA interference (RNAi) assay to assess the inheritance of gene silencing. Parent animals are subjected to an RNAi trigger to silence a germline 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. This study examines the impact of the highly homologous genes set‑9 and set‑26, as well as a third similar gene termed Y73B3A.1, on TEI. The results of the study implicate all three as having roles in the establishment of a heritable silencing signal and show set‑26 also acts to maintain this signal through multiple generations. Both SET‑9 and SET‑26 have a SET domain and a PHD finger, shown to bind H3K4me3. Our results suggest that both domains are involved in the establishment of TEI, but that only the PHD finger of SET‑26 impacts the maintenance of gene silencing through successive generations, implicating chromatin regulation as pivotal for TEI. Our results also suggest that parent animals require working copies of set‑9 and Y73B3A.1 to properly establish a heritable silencing signal within their progeny.