KIF11, a member of the kinesin family, plays a critical role in mitosis by forming and maintaining the bipolar spindle. Abnormal KIF11 expression is associated with cancer progression, and its upregulation has been observed in various cancers, including glioma, adrenocortical carcinoma, colorectal cancer, non-small-cell lung cancer, and hepatocellular carcinoma. KIF11 promotes cancer proliferation, invasion, and metastasis by regulating cell signaling pathways and is involved in key cancer hallmarks such as epithelial-mesenchymal transition and angiogenesis. It is also regulated at the transcriptional, post-transcriptional, and post-translational levels in tumorigenesis and tumor progression. KIF11 inhibitors have been developed, but their effectiveness varies, and resistance mechanisms, such as mutations in the loop 5 region, can limit their efficacy. KIF11 inhibitors induce mitotic arrest and aberrant monopolar spindles with minimal neurotoxicity, making them a promising therapeutic target. However, potential risks, such as neurotoxic effects and complications with learning ability and memory, must be considered. KIF11's functions during mitosis include centrosome events, spindle events, and interactions with binding partners like NuMA and TPX2. Dysregulated KIF11 expression is linked to poor prognosis in several cancers, and its clinical relevance is supported by studies showing its association with various clinicopathological features. KIF11's regulation involves transcriptional, post-transcriptional, and post-translational mechanisms, including phosphorylation, acetylation, and ubiquitination. KIF11's oncogenic functions include promoting cancer proliferation, invasion, and metastasis through various signaling pathways. KIF11 inhibitors are being explored for clinical trials, but their effectiveness in different cancers remains a challenge. Future research should focus on understanding KIF11's role in the cancer microenvironment, its interactions with other proteins, and its non-mitotic functions in neurons. KIF11 inhibition may also have therapeutic potential in neurological disorders and cancer pain management.KIF11, a member of the kinesin family, plays a critical role in mitosis by forming and maintaining the bipolar spindle. Abnormal KIF11 expression is associated with cancer progression, and its upregulation has been observed in various cancers, including glioma, adrenocortical carcinoma, colorectal cancer, non-small-cell lung cancer, and hepatocellular carcinoma. KIF11 promotes cancer proliferation, invasion, and metastasis by regulating cell signaling pathways and is involved in key cancer hallmarks such as epithelial-mesenchymal transition and angiogenesis. It is also regulated at the transcriptional, post-transcriptional, and post-translational levels in tumorigenesis and tumor progression. KIF11 inhibitors have been developed, but their effectiveness varies, and resistance mechanisms, such as mutations in the loop 5 region, can limit their efficacy. KIF11 inhibitors induce mitotic arrest and aberrant monopolar spindles with minimal neurotoxicity, making them a promising therapeutic target. However, potential risks, such as neurotoxic effects and complications with learning ability and memory, must be considered. KIF11's functions during mitosis include centrosome events, spindle events, and interactions with binding partners like NuMA and TPX2. Dysregulated KIF11 expression is linked to poor prognosis in several cancers, and its clinical relevance is supported by studies showing its association with various clinicopathological features. KIF11's regulation involves transcriptional, post-transcriptional, and post-translational mechanisms, including phosphorylation, acetylation, and ubiquitination. KIF11's oncogenic functions include promoting cancer proliferation, invasion, and metastasis through various signaling pathways. KIF11 inhibitors are being explored for clinical trials, but their effectiveness in different cancers remains a challenge. Future research should focus on understanding KIF11's role in the cancer microenvironment, its interactions with other proteins, and its non-mitotic functions in neurons. KIF11 inhibition may also have therapeutic potential in neurological disorders and cancer pain management.