RHOQ is a plasma membrane-associated small GTPase that cycles between active GTP-bound and inactive GDP-bound states to regulate cellular responses 1. It functions in epithelial cell polarization and filopodia formation through actin cytoskeletal reorganization, with roles in membrane trafficking and insulin-stimulated glucose uptake 1. Mechanistically, RHOQ regulates angiogenesis by controlling Notch intracellular domain nuclear translocation; loss of RHOQ results in NICD degradation via autophagy and lysosomal pathways, impairing DLL4/Notch signaling 2. Clinically, RHOQ dysregulation associates with multiple diseases. In lung adenocarcinoma, RhoQ acts as a negative regulator of TGF-β-mediated epithelial-mesenchymal transition; low RhoQ levels correlate with poor overall survival 1. In colorectal cancer, RNA editing-mediated RhoQ N136S substitution increases protein activity and invasion potential, with edited RHOQ transcripts and KRAS mutations predicting recurrence 3. RHOQ emerges as a potential Alzheimer's disease biomarker, identified among top dysregulated genes in large-scale AD expression analysis 4, with differential expression in AD cell models and identified as a feature gene in necroptosis-related AD subtypes 5, 6. CDC42 family inhibitors targeting RHOQ interactions show promise for cancer treatment by blocking tumor growth and angiogenesis 7.