The Wiskott-Aldrich syndrome (WAS) protein family shares a common domain structure and links signals from cell surface receptors to the actin cytoskeleton. Their diverse motifs suggest regulation by multiple stimuli and interactions with various proteins. These proteins associate with the small GTPase Cdc42, which regulates actin filament formation, and the Arp2/3 complex, a key cytoskeletal organizer. WAS is a rare X-linked recessive disorder marked by immune dysregulation and microthrombocytopenia, caused by mutations in the WAS gene. The WAS protein is cytoplasmic and expressed only in hematopoietic cells, which exhibit signaling and cytoskeletal defects in patients. An alternative transcript variant with a different 5 UTR has been reported, though its full-length sequence remains unclear.