FAM107A is a stress-inducible actin-binding protein with dual roles in neural development and tumor suppression. In the nervous system, FAM107A regulates actin filament dynamics and is preferentially expressed in outer radial glia, neural stem cells critical for human cortical expansion 1. The protein mediates F-actin polymerization, stabilization, and bundling, functions essential for synaptic plasticity and cognitive processes. Clinically, FAM107A functions as a tumor suppressor across multiple malignancies. In laryngeal squamous cell carcinoma, FAM107A undergoes recurrent inactivation through combined chr3 loss (3p deletion) and promoter hypermethylation, with Decitabine restoring expression 2. Similar downregulation occurs in non-small cell lung cancer 3, esophageal squamous cell carcinoma 4, and bladder cancer 5, where FAM107A suppression correlates with poor prognosis and advanced tumor staging. Mechanistically, FAM107A inhibits cancer progression through multiple pathways: in colorectal cancer, it suppresses epithelial-mesenchymal transition via AKT pathway inhibition 6 and operates within a DNMT1/FAM107A/FOXM1 regulatory axis controlling proliferation and apoptosis 7. Diagnostically, IQGAP3/FAM107A expression ratios in urinary cell-free DNA effectively discriminate bladder cancer from hematuria with 88.6% specificity 8. These findings establish FAM107A as a promising tumor suppressor and therapeutic target across cancers.