FILIP1L is a tumor suppressor-like protein that functions as a negative regulator of cell proliferation and angiogenesis across multiple cancer types. Mechanistically, FILIP1L inhibits the canonical Wnt/β-catenin signaling pathway, reducing β-catenin-mediated transcription of oncogenic targets 1. In colorectal cancer, FILIP1L suppresses tumor cell migration, invasion, and angiogenesis while promoting apoptosis and cell cycle arrest; its expression correlates with improved prognosis and reduced tumor progression 2. FILIP1L expression is downregulated in various cancers through promoter methylation, including lung adenocarcinoma where loss promotes mucin production and inflammation 3. Beyond cancer, FILIP1L plays a physiological role in muscle homeostasis: the exercise-induced myokine Musclin upregulates FILIP1L through FoxO3a transcription, promoting fibro-adipogenic progenitor apoptosis and preventing fibrosis and fatty infiltration in injured muscles 4. In bladder cancer, the TDO2/AhR pathway upregulates FILIP1L alongside SPARC, though the functional consequences remain unclear 5. Recently, FILIP1L was identified as regulating macrophage cholesterol metabolism in atherosclerosis, where overexpression reduces oxLDL accumulation 6. FILIP1L localizes to the actin cytoskeleton and regulates centrosomal protein stability through binding prefoldin 1 7. Its therapeutic restoration represents a promising approach for cancer and degenerative muscle diseases.