GNG7 encodes the G protein subunit gamma 7, a component of heterotrimeric G-protein complexes essential for G protein-coupled receptor signaling and adenylyl cyclase regulation in specific brain regions [UniProt]. GNG7 functions as a critical component of G(olf) heterotrimer formation required for striatal adenylyl cyclase activity [UniProt]. Mechanistically, GNG7 participates in transmembrane signaling through beta-gamma chain interactions that facilitate GTPase activity and G protein-effector interactions [UniProt]. Clinically, GNG7 acts as a tumor suppressor across multiple cancer types. GNG7 is consistently downregulated in pancreatic adenocarcinoma, head and neck squamous cell carcinoma, gastric cancer, and clear cell renal cell carcinoma 1234. In head and neck cancer, GNG7 inactivation occurs primarily through promoter hypermethylation (43% of tumors), correlating with tumor size 2. GNG7 downregulation associates with poor overall survival and serves as an independent prognostic risk factor across multiple malignancies 135. GNG7 overexpression inhibits cancer cell proliferation, colony formation, and cell cycle progression while inducing apoptosis 34. Beyond cancer, GNG7 is upregulated in preeclampsia placental tissues, where elevated expression impairs trophoblast migration and invasiveness 6. In acne pathogenesis, miR-146a suppresses GNG7 expression, promoting sebocyte lipid production 7. These findings establish GNG7 as a potential diagnostic, prognostic biomarker, and therapeutic target across multiple diseases.