Cell cycle control in mammalian cells consists of inherent mechanisms that prevent aberrant proliferation leading to cellular transformation. Such mechanisms include DNA damage detection and repair to regulate chromosome integrity, as well as cell cycle checkpoints. Recent evidence suggests that Brit1 is involved in such mechanisms of cell cycle control. Initially identified as a suppressor of telomerase activity, Brit1’s function as a potential tumor suppressor was supported after its role as a mediator of the DNA damage response (DDR) pathway was detailed. DNA damage in the form of single or double strand breaks leads to Brit1 localization to the damaged site. This is followed by Brit1-mediated recruitment and activation of regulatory proteins that transduce the damage signal to activate cell cycle checkpoints. Specifically, following a DNA double stranded break (DSB), Brit1 co-localizes with γ-H2AX, followed by subsequent recruitment of ATM, ATR, 53BP1, MDC1 and NBS1 proteins. It was shown that Brit1 interaction with SWI/SNF is required for this recruitment process and IR-induced foci (IRIF) formation. Beyond its role in the DNA damage response, Brit1 has also been shown to play a central role in maintaining centrosome copy number, and regulating the timing of chromosome condensation through its interaction with condensin II. Accumulating research suggests that Brit1 is a tumor suppressor, as evidenced by an inverse relationship between Brit1 expression and chromosomal abnormalities observed in human breast cancer cell lines and ovarian and prostate tumors. Furthermore, Brit1 has been shown to be a prognostic marker used to predict breast tumor grade.