FMNL3 (formin-like 3) is a cytoskeletal regulator that controls cell morphology and migration through actin filament organization 1. As an FDD-type formin homology protein containing FDD, FH1, and FH2 domains 1, FMNL3 functions in coordinating actin cytoskeleton dynamics and filopodium assembly. Beyond developmental angiogenesis, FMNL3 plays a critical pro-metastatic role in cancer. In breast cancer, elevated FMNL3 expression promotes cell migration and invasion by stabilizing Twist1 protein, which suppresses E-cadherin (CDH1) transcription and drives epithelial-mesenchymal transition (EMT) 2. Similarly, in nasopharyngeal carcinoma, FMNL3 overexpression induces TGF-β1-mediated EMT and correlates with advanced clinical stage, lymph node metastasis, and distant metastasis 3. Gene-based association studies identified FMNL3 as a novel breast cancer susceptibility gene 4, with high expression linked to poor prognosis across multiple cancer types 1. FMNL3 appears implicated in cancer progression through the Rho-related signaling pathway, positioning it as both a potential biomarker and therapeutic target for metastatic malignancies.