Although formal demonstration of elevated MycCMG interactions in tumor cells versus non-tumor cells has not been shown experimentally, but could be addressed using ChIPseq based approaches, it is known from several studies that overexpression of Myc does indeed produce an increase in replication origin usage and CMG helicase over-activation,[18–20] consistent with the mechanisms underlying Myc stimulation of CMG assembly. This evidence concerns the gene MYC and neoplasm.