Understanding how effector proteins recognise and influence the spread of epigenetic marks is relatively novel, where in C. elegans, Su(var)3-9, Enhancer of Zeste, Trithorax (SET)-domain containing proteins interact with epigenetic marks(Ni et al., 2012). SET-9 and SET-26 are two such effector proteins, recognising the active H3K4me3 mark, and when ineffective we observe the spreading of these H3K4me3 marks(Pu et al., 2018). Both proteins contain a non-catalytically active SET-domain, which when functional is known to perform methyltransferase activity on histones. These two proteins share 97% sequence homology, but SET-9 appears to solely function in the germline of C. elegans, whereas SET-26 functions in both the soma and the germline(Monteiro, 2023; Pu et al., 2018). Using CUT&RUN, mRNA-seq and sRNA-seq we can observe a restriction function in which mutants of SET-9 and SET-26 are unable to regulate the spread of H3K4me3 in the germline to inactive chromatin, indicating a regulatory role for these proteins at chromatin borders. The spreading of active H3K4me3 in the germline has some impact on mRNA and sRNA production, from which SET-9 mutants are most similar to WT, indicating loss of function of SET-26 has a drastic effect on the epigenome.