GABRP encodes the pi subunit of GABA type A receptors, heteropentameric ligand-gated chloride channels activated by gamma-aminobutyric acid 1. In normal physiology, GABRP-containing receptors are predominantly expressed in peripheral tissues, including the uterus where they modulate contraction by altering sensitivity to pregnanolone 2. However, GABRP is aberrantly upregulated in multiple cancers including pancreatic ductal adenocarcinoma, gliomas, and breast cancer, where it functions atypically 34. Rather than acting as a conventional ionotropic chloride channel at physiological GABA concentrations, GABRP instead activates G-protein-coupled signaling pathways leading to ERK activation and tumor progression 5. In pancreatic cancer, GABRP interacts with KCNN4 to induce calcium entry, activating NF-κB signaling and promoting macrophage infiltration through CXCL5 and CCL20 expression 3. GABRP also mediates gemcitabine resistance via CD44s-dependent mechanisms and contributes to immunosuppressive tumor microenvironments by recruiting regulatory T cells and M2 macrophages 64. In pregnancy-related pathology, increased GABRP expression in preeclampsia promotes trophoblastic apoptosis and impairs cell invasion 7, while reduced GABRP in gestational diabetes mellitus decreases trophoblast viability and migration 8. These findings establish GABRP as a therapeutic target in cancer and placental disorders.