JTB (jumping translocation breakpoint) is a regulator of cell division required for normal cytokinesis during mitosis. It functions as a component of the chr1 passenger complex (CPC), which controls centromeric functions essential for proper chromosome 1 and segregation. JTB enhances AURKB kinase activity and promotes microtubule stabilization and spindle assembly during mitosis. The protein also inhibits apoptosis and, when overexpressed, induces mitochondrial swelling and reduces mitochondrial membrane potential. JTB is implicated in multiple cancers, including cervical carcinoma, hepatocellular carcinoma, and glioblastoma multiforme, consistent with its pro-proliferative and anti-apoptotic roles. Additionally, JTB has been associated with neurodegenerative conditions such as Alzheimer disease and Huntington disease, though the mechanisms in these contexts remain incompletely characterized. Its involvement in cell cycle regulation and apoptosis suppression positions JTB as a potential target for cancer intervention, though no specific therapeutic agents targeting JTB have been validated in clinical trials to date.