It therefore can be inferred that part of MYC’s oncogenic potential is mediated indirectly through the action of CCAT1 and PVT1. These findings support a role of CCAT1 and PVT1 as dominant oncogenes in AML and suggest that interference with the function of these lncRNAs could represent a new therapeutic tool against MYC driven hematological malignancies (124). This evidence concerns the gene MYC and acute myeloid leukemia.