XPO7 (exportin 7) is a broad-spectrum bidirectional nucleocytoplasmic transporter that mediates nuclear export of ~200 protein cargoes and unexpectedly also functions as a nuclear import receptor for ~30 substrates 1. XPO7 binds cargo cooperatively with RanGTP in the nucleus; upon nuclear pore complex transit, RanGTP hydrolysis releases cargo into the cytoplasm, enabling recycling of XPO7 to the nucleus 2. XPO7 functions as a context-dependent regulator with dual roles in cancer. In TP53-wild-type cells, XPO7 acts as a tumor suppressor by regulating p53 nuclear abundance and promoting p21CIP1-mediated senescence 2. However, in TP53-mutated acute myeloid leukemia, XPO7 drives leukemia proliferation by retaining the nuclear protein NPAT, promoting histone loss and genomic instability 3. High cytoplasmic XPO7 expression independently predicts poor overall survival in high-grade serous ovarian cancer 4. Beyond cancer, XPO7 participates in multiple physiological processes: it modulates erythrocyte traits through IKZF1-mediated regulation 5, contributes to circadian rhythm regulation via E-box protein interactions 6, shares genetic overlap with cardiovascular disease and telomere maintenance 7, and haploinsufficiency increases schizophrenia risk through disrupted nuclear transport and gene expression patterns in frontal cortex circuits 8.