WIPF1 (WAS/WASL interacting protein family member 1) is a cytoskeletal regulator that plays a central role in actin polymerization and cell motility. As an adaptor protein, WIPF1 recruits and activates WASL (N-WASP) in conjunction with NCK1 and GRB2, promoting the reorganization of the actin cytoskeleton from stress fibers toward filopodia and cell ruffles formation 1. WIPF1 coordinates these cytoskeletal dynamics through interaction with ACTN4 to regulate podosome formation and matrix degradation 2. In pregnancy, WIPF1 is exclusively expressed in placental extravillous trophoblasts (EVTs) where it critically regulates cell migration and trophoblast differentiation; reduced WIPF1 levels correlate with recurrent spontaneous abortion (RSA) pathogenesis 2. WIPF1 mutations cause Wiskott-Aldrich Syndrome 2, characterized by immunodeficiency and cytoskeletal abnormalities 1. In immune cells, WIPF1 deficiency impairs T-cell receptor signaling and promotes aberrant B-cell activation leading to intestinal inflammation 3. Clinically, WIPF1 functions as an oncoprotein in multiple cancers. Elevated WIPF1 promotes invasion and metastasis in pancreatic ductal adenocarcinoma via the miR-141/200c-WIPF1-YAP/TAZ pathway and associates with poor survival 4. In papillary thyroid cancer, BRAF V600E-induced WIPF1 upregulation drives aggressive phenotypes including lymph node metastasis 5. WIPF1 overexpression is also prognostically unfavorable in colorectal cancer, glioma, and breast cancer 6.