Most human cancers have been found to have gains and losses of chromosomes that may be due to chromosomal instability (CIN). One of the things that cause CIN is the inactivation of genes that control the proper segregation of the sister chromatids during mitosis. In gaining a better understanding of survivin's function in mitotic regulation, scientists have looked into the area of genomic instability. It is known that survivin associates with microtubules of the mitotic spindle at the start of mitosis.
It has been shown in the literature that knocking out survivin in cancer cells will disrupt microtubule formation and result in polyploidy as well as massive apoptosis. It has also been shown that survivin-depleted cells exit mitosis without achieving proper chromosome alignment and then reforms single tetraploid nuclei. Further evidence also suggests that survivin is needed for sustaining mitotic arrest upon encounter with mitosis problems. The evidence mentioned above implicates that survivin plays an important regulatory role both in the progression of mitosis and sustaining mitotic arrest. This seems strange, as survivin is known to be highly upregulated in most cancer cells (that usually contain chromosome instability characteristics), and its function is that which promotes proper regulation of mitosis.