Multiple studies reveal functional interactions between MYC and PVT1. For example, MYC and PVT1 are almost always co-amplified in cancers that exhibit somatic copy number gains at 8q24, and mouse models have been used to demonstrate that a single copy gain of a chromosome segment harboring Myc and Pvt1 enhances mammary tumorigenesis driven by an MMTV-NEU transgene, whereas single copy gains of Myc or Pvt1 alone do not [69]. This evidence concerns the gene MYC and cancer.