PREX1 is a RAC guanine nucleotide exchange factor (GEF) that activates RAC proteins by catalyzing GDP-to-GTP exchange, with activity synergistically enhanced by phosphatidylinositol 3,4,5-trisphosphate and G protein βγ subunits [UniProt]. It regulates actin filament polymerization and neutrophil activation through small GTPase signaling [GO Annotations]. In cancer biology, PREX1 plays multifaceted roles across tumor types. In acute myeloid leukemia, PREX1 functions as a Ras-dependent activator of MAPK signaling 1. In colorectal cancer, an enhancer variant (rs4810856) distally regulates PREX1 expression to activate p-AKT signaling 2. In gastric cancer, PREX1 silencing inhibits transforming growth factor-β1-induced epithelial-mesenchymal transition and promotes apoptosis 3. In osteosarcoma, elevated PREX1 expression in metastatic tumors promotes proliferation, invasion, and migration, with PREX1 loss reducing these malignant capacities 4. Beyond cancer, PREX1 exhibits immunoregulatory functions: it promotes STAT5 nuclear translocation in response to IL-7, enhancing homeostatic proliferation of naive CD4+ T cells during aging 5. PREX1 genetic variants associate with preeclampsia susceptibility, suggesting roles in vascular biology and pregnancy physiology 6.