In other primary cancer cells, pri-Can-2 and pri-Can-3, as well as in established CRC cell lines (HT-29 and HCT-116), stable NSD2 silencing by the shNSD2-Seq-1 (see Fig. 2) similarly increased caspase-3 activity (Fig. 3G) and induced mitochondrial depolarization (JC-1 green monomers accumulation, Fig. 3H). This evidence concerns the gene NSD2 and colorectal carcinoma.