Analysis of data from The Cancer Genome Atlas (TCGA) database revealed that a co-gain of both MYC and PVT1 in almost all (98%) tumors showing 8q24 copy-number increases, whereas very few (0.15%) tumors showed an increase in copy number of MYC alone without PVT1. CRISPR Cas9-mediated disruption of PVT1 in MYC dependent HCT116 colon cancer cells significantly reduced its tumorigenic potency suggesting that PVT1 regulates the activity of MYC as an oncogene (70) or even act as an oncogene independently of MYC (103). Here, PVT1 is linked to colonic neoplasm.