Conversely, we established that the transcriptional status of NIPSNAP1 was dependent upon the repressive activity of c-Myc-Miz1, with de-repression occurring following serum withdrawal resulting in the transactivation of NIPSNAP1. Notably, antagonizing the induction of NIPSNAP1 was revealed to have important consequences regarding cell fate wherein cancer cells not only decreased their proliferation but were triggered to enter senescence through increases in the expression of P27. This evidence concerns the gene NIPSNAP1 and cancer.