KCTD17 is a substrate adapter for CUL3-RING ubiquitin ligase complexes that regulates protein degradation through multiple pathways. Its primary established function involves promoting ciliogenesis by mediating TCHP degradation, thereby facilitating axoneme extension 1. KCTD17 may also influence endoplasmic reticulum calcium homeostasis 2. Recent research has expanded understanding of KCTD17's pathological roles. In hepatocellular carcinoma, KCTD17 promotes tumor progression by degrading Lztr1, a Ras destabilizer, leading to Ras stabilization and enhanced cellular proliferation and migration 3. In metabolic dysfunction-associated steatohepatitis, KCTD17 facilitates Zbtb7b degradation, reducing SERPINA3 expression and promoting hepatic fibrosis through PAR2/TGFβ signaling 4. In obesity-induced metabolic disease, KCTD17 degrades O-GlcNAcase, stabilizing ChR22 and exacerbating glucose intolerance and hepatic steatosis 5. KCTD17 demonstrates functional redundancy with related KCTD proteins in controlling cellular growth 6. Clinically, mutations in KCTD17 cause dystonia 26 with myoclonus, a primary monogenic movement disorder 7. KCTD17 represents an emerging therapeutic target for hepatocellular carcinoma, fatty liver disease, and metabolic complications of obesity, with antisense oligonucleotides showing promise in preclinical models 35.