[citation needed] However, recent evidence implicates TRIP13 in various cell cycle phases, including meiosis G2/Prophase and during the Spindle Assembly checkpoint (SAC).

[5] Of note, Mad2's involvement in the SAC is shown to be affected by TRIP13 [6] Due to TRIP13's role in cell cycle arrest and progression, it may present opportunity as a therapeutic candidate for cancers.

[8] TRIP13/PCH2 interacts with ATP as a hydrolase, hydrolyzing phosphates to derive energy for conformational changes that can induce mechanical force on its substrate, Hop1 in the previous case.

The homologous recombination that occurs following these breaks requires a protein complex to influence and structure appropriate chromosomal pairing.

Without TRIP13, meiocytes had pericentric synaptic forks, fewer crossovers, and altered distribution of chiasma (the contact point between homologous chromosomes.

[14] Research shows a robust and varied role for TRIP13/PCH2 to remove various proteins for SC formation, thus allowing meiosis to continue.

[5] To continue from metaphase to anaphase, the cell must ensure chromosomes are bioriented and properly structured in order for correct and error-free separation of sister chromatids.

Experiments in human HeLa and HCT116 cells show that neither p31-Comet nor TRIP13 was particularly required for unperturbed mitosis, and that depleting P31-Comet only slightly impaired Mad2 inactivation.

In one instance, overexpression of TRIP13 has been shown to affect treatment resistance for Squamous cell carcinoma of the head and neck.