Given that tumour formation was seen in a cell line with non-functional p53, and Spy1 can prevent checkpoint activation [13, 15, 16, 20], it is plausible then that wild-type p53 may work to downregulate Spy1 to allow for p53-mediated cell cycle arrest, and elevated Spy1 with loss of p53 function would allow for enhanced genomic instability. Here, SPDYA is linked to neoplasm.