SUGT1 (suppressor of G2 allele of SKP1) functions as a molecular cochaperone essential for kinetochore assembly and cell cycle progression through G1/S and G2/M transitions 1. The protein stabilizes microtubule plus-ends through modulation of microtubule acetylation and EB1 comet formation 2, and regulates protein stability via ubiquitin-proteasome-mediated degradation pathways 3. Mechanistically, SUGT1 promotes FH protein degradation to activate PI3K/AKT signaling 3. Clinically, SUGT1 overexpression is associated with poor prognosis across multiple cancers. In colorectal cancer, high SUGT1 expression with genomic amplification correlates with elevated recurrence frequency and diminished survival 4. Similarly, in ovarian cancer, SUGT1 serves as an independent prognostic risk factor linked to shorter overall survival, disease-specific survival, and progression-free interval, with associations to altered immune infiltration patterns including reduced cytotoxic T cells 1. SUGT1 promotes ovarian cancer proliferation and migration through FH downregulation 3. Beyond malignancy, genome-wide association studies identified SUGT1 as a candidate susceptibility gene for irritable bowel syndrome 5, and it participates in ulcerative colitis pathogenesis via the CBR3-AS1/KLF2/SUGT1 pyroptosis pathway 6. Additionally, SUGT1 enhances HIV-1 permissiveness by facilitating nuclear import and retrograde trafficking 2.