The epigenome is a complex framework through which precise gene expression takes place. Epigenome is one of the key regulators of cell fate, certain diseases, and aging. Editing the epigenome is a promising therapeutic approach in cancer. For epigenome editing, a 'dead' Cas9 protein (dCas9) is used that lacks nuclease activity, and it is places alongside an epigenetic effector domain. Based on fusion partners of dCas9, an exact epigenetic status can be achieved. Granulin (GRN), is upregulated in hepatoma tissues and is associated with decreased tumor survival in patients with hepatoma. It is a growth factor and a potent pluripotent mitogen that promotes cancer progression by maintaining self-renewal of hepatic stem cancer cells. Wang et al. synthesized a set of dCas9 epi-suppressors to target GRN by tethering the C terminus of dCas9 with three epigenetic suppressor genes: DNMT3a (DNA methyltransferase), EZH2 (histone 3 lysine 27 methyltransferase), and KRAB (the Krüppel-associated box transcriptional repression domain). The epigenetic knockdown of GRN (by altering promoter methylation status) led to the inhibition of cell proliferation, decreased tumor sphere formation, and reduced cell invasion. The mutated transcription factor FOXA1 acts as an oncogene and is responsible for the onset and progression of prostate cancer. identified a group of six cis-regulatory elements in the FOXA1 regulatory plexus containing somatic single-nucleotide variants in primary prostate tumors. Deletion and repression of these cis-regulatory elements with the help of CRISPR/Cas technology, significantly decreases FOXA1 expression and prostate cancer cell growth.