FKBP10 (FK506 binding protein 10) is a peptidyl-prolyl cis-trans isomerase (PPIase) localized to the endoplasmic reticulum that accelerates protein folding during synthesis 1. Primary mutations in FKBP10 cause Bruck syndrome 1 and osteogenesis imperfecta 11, with documented gross deletions identified in Chinese OI patients 2. Beyond its classical role in protein folding, FKBP10 exhibits multifaceted oncogenic functions across multiple cancer types. In clear cell renal cell carcinoma (ccRCC), FKBP10 promotes progression and glycolytic metabolism by directly binding lactate dehydrogenase A (LDHA) through its C-terminal region and enhancing LDHA phosphorylation, driving the Warburg effect and histone lactylation 1. In ccRCC, FKBP10 also activates the IL-6/JAK/STAT3 pathway to promote malignant phenotypes 3. In bladder cancer, FKBP10 promotes muscle invasion and metastasis by interacting with prelamin A, preventing its nuclear entry and reducing nuclear lamin A levels, thereby increasing nuclear atypia 4. FKBP10 expression is associated with poor prognosis in gastric adenocarcinoma and pituitary adenomas and correlates with an immunosuppressive tumor microenvironment 56. These findings suggest FKBP10 inhibition may enhance HIF2α inhibitor efficacy and provide therapeutic opportunities across multiple malignancies.