TMSB10 (thymosin beta 10) is a cytoskeletal regulatory protein that binds and sequesters actin monomers (G-actin), inhibiting actin polymerization and regulating cell migration. Beyond its canonical role in cytoskeletal organization, TMSB10 has emerged as a significant oncogenic factor across multiple cancer types. In prostate cancer, high TMSB10 expression correlates with poor patient outcomes and promotes tumor aggressiveness by suppressing cell proliferation, migration, and invasion when silenced 1. TMSB10 modulates the tumor immune microenvironment by skewing macrophage polarization toward M2-type phenotypes, reducing immune cell cytotoxicity 1. Similar oncogenic roles are observed in glioma, where TMSB10 upregulation associates with advanced histological grades and worse survival 2, and in clear cell renal cell carcinoma, where JUN transcription factor regulates TMSB10 expression to promote proliferation and inhibit apoptosis 3. In non-small-cell lung cancer, TMSB10 degradation via the autophagy-lysosome pathway disrupts F-actin formation and cell migration 4. In gastric cancer, TMSB10 overexpression promotes invasion and angiogenesis 5. Beyond malignancy, TMSB10 is upregulated in acute pancreatitis as an immune-associated gene signature 6 and in cerebrospinal fluid of both autosomal dominant and sporadic Alzheimer's disease, potentially serving as a novel biomarker 7. These findings establish TMSB10 as a multifunctional protein with therapeutic potential across diverse diseases.