the protein, inhibits Bcl-2 and Bcl-xL proteins that produce the anti-apoptotic activity in the mitochondria, thereby promoting cell death. During stressful conditions that damage DNA, tyrosine kinase C-Abl activates the BH3 motif by phosphorylating Y38, the tyrosine located in the BH3 motif, which promotes rad-9 Bcl-xL binding that induces apoptosis. Role in tumorigenesis The somatic mutations that an organism accumulates over a life-time, alongside the various chemicals one is exposed to, gives rise to cancer. Given Rad-9’s extensive role in cell cycle inhibition as part of the 9-1-1 complex and its interactions with proteins responsible for DNA repair, it can be reasonably inferred that Rad-9 has many tumor suppressive roles, where its loss of function leads to tumorigenesis. The tumor suppressive aspect of Rad-9 can also be seen from its crucial functions in activating apoptosis in the case of extensive DNA damage. Given its key role, impactful Rad-9 mutations can give rise to cancer. However, the complexity of the protein’s interactions is evident as Rad-9 overexpression has been linked to many forms of lung and prostate cancers. Furthermore, a number of research studies have found that the Rad-9 protein was necessary for the survival of the tumor cells. Due to the high mutation rate, replication stalls, and overall replicative stress, tumor cells are heavily reliant on DNA damage mechanisms to keep up with the division rate demands. Given these recent findings, Rad-9 has been described as a dual function protein with oncogenic properties that are necessary for the growth of specific tumor cells on the one hand, and with tumor suppressive properties that are necessary for the control of normal cell growth. Future research about the oncogenic properties of Rad-9 are necessary to reveal the full complexity of this protein and its importance to the cell cycle control system. History Rad9 was first found as a gene that promotes G2 cell cycle arrest in response to DNA damage in Saccharomyces cerevisiae by Weinert et al. The group irradiated yeast cells to induce DNA damage and tested many different mutants. They tested 7 rad mutants and all of the mutants underwent G2 arrest as normal, except for one, the rad9 mutant. The rad9 mutant did not undergo G2 arrest and instead proceeded through the cell cycle and many of the cells died because the DNA was never repaired. From this they suspected that Rad9 is necessary to invoke G2 cell cycle