CRACD (capping protein inhibiting regulator of actin dynamics) functions as a critical regulator of actin cytoskeleton dynamics with tumor suppressor properties. The protein promotes actin polymerization by inhibiting capping protein interactions with actin filaments, thereby maintaining epithelial cell integrity 1. CRACD stabilizes the cadherin-catenin-actin complex, and its loss disrupts this complex leading to β-catenin release and Wnt signaling hyperactivation 1. In cancer contexts, CRACD frequently shows reduced expression or mutations across multiple tumor types. CRACD loss drives neuroendocrine plasticity in lung cancers by disrupting actin organization, which suppresses Yap1-NOTCH signaling and promotes neuroendocrine gene expression 23. Additionally, CRACD inactivation leads to EZH2-mediated histone methylation and MHC-I gene repression, facilitating immune evasion 2. In colorectal cancer, decreased CRACD expression correlates with increased stemness, metastasis, and poor prognosis through YAP-mediated pathways 4. Paradoxically, some studies report CRAD as oncogenic in lung cancer, where knockdown suppresses growth and promotes apoptosis via Claudin 4 regulation 5. These findings establish CRACD as a multifunctional cytoskeletal regulator with complex, context-dependent roles in cancer biology.