VIL1 (villin 1) is an epithelial cell-specific actin-modifying protein that regulates intestinal brush border cytoskeleton organization and cell differentiation. Functionally, VIL1 modulates microvillar actin filament dynamics through nucleation, bundling, capping, and severing activities in a calcium-dependent manner 1. These actin-regulatory functions are critical for maintaining epithelial barrier integrity—butyrate co-treatment with the mycotoxin deoxynivalenol partially restored VIL1 expression and reduced epithelial dysfunction 2. VIL1 plays important roles in intestinal homeostasis and disease pathogenesis. In infection models, VIL1's actin-severing activity enhances pathogen dissemination, while its baseline expression protects against apoptosis in gastrointestinal inflammation. Notably, Helicobacter pylori's HpSlyD protein induces VIL1 expression through TCTP-mediated signaling, contributing to intestinal metaplasia development in the stomach 3. In cancer biology, VIL1 expression is significantly upregulated in colorectal cancer (CRC) tissues compared to normal tissue 4. VIL1 promotes CRC progression by activating the NF-κB pathway and inhibiting ferroptosis, while VIL1 knockout suppresses proliferation and induces ferroptosis-mediated cell death 4. Additionally, VIL1 serves as a diagnostic biomarker—the miR-192-5p/HNF1A-AS1/VIL1 panel achieved 91.1% accuracy in cervical adenocarcinoma diagnosis 5, and VIL1 combined with CDX2 shows 81% specificity for distinguishing large-cell neuroendocrine carcinomas 6.