KANK1 is an adapter protein that organizes cortical microtubule-stabilizing complexes at focal adhesions and regulates cytoskeleton dynamics 1. It links microtubule and actin networks by interacting with talin and recruiting KIF21A, thereby controlling microtubule-actin crosstalk at cell edges and guiding axon growth 1. KANK1 inhibits RhoA activation and lamellipodium formation through PI3K/Akt signaling and 14-3-3 protein sequestration, thereby suppressing cell migration 2. Optogenetic activation of KANK1-mediated microtubule/talin linkage promotes focal adhesion disassembly via GEF-H1/RhoA/ROCK-dependent contractility 3. KANK1 participates in Wnt/β-catenin-dependent transcription in the nucleus 4. Mutations in KANK1 cause spastic cerebral palsy through axonal dysfunction and TDP-43 mislocalization in motor neurons, highlighting its ALS disease relevance 5. The clinical significance of KANK1 is paradoxical: while upregulation suppresses lung, gastric, and brain glioma cancer progression through apoptosis and cell-cycle arrest 678, high KANK1 expression associates with poor breast cancer prognosis by competing with Scribble for Hippo pathway inhibition 9. Low KANK1 expression correlates with poor pulmonary adenocarcinoma prognosis 10, suggesting tissue-specific tumor suppressor or oncogenic roles.