FIGN (fidgetin) is an ATP-dependent microtubule-severing protein that regulates cytoskeletal dynamics through its conserved AAA+ domain 1. The protein contains a nuclear localization signal (residues 314-323) essential for nuclear translocation, where it preferentially severs highly-tyrosinated microtubules and regulates microtubule polymer configuration 2. FIGN participates in cell division and neuronal regeneration, with functional roles extending beyond microtubule severing 1. In disease contexts, FIGN exhibits paradoxical associations. In hepatocellular carcinoma, high FIGN expression correlates with tumor progression, shorter overall survival, microvascular invasion, and portal vein thrombosis, suggesting prognostic value as a negative prognostic marker 34. Conversely, FIGN variants show protective effects against congenital heart disease: the rs2119289 C allele increases FIGN expression, promoting folate absorption and metabolism while reducing CHD risk by 44-66% depending on genotype 56. A PCOS genome-wide association study identified the KCNH7/FIGN locus associated with metabolic PCOS subtype 7. Additionally, FIGN exhibits sex-specific DNA methylation changes during aging, with implications for longevity and age-related disease susceptibility 8. These findings suggest FIGN functions as both a therapeutic target in cancer and a biomarker for metabolic and developmental disorders.