ZDHHC7 is a Golgi-localized palmitoyltransferase that catalyzes the addition of palmitate to diverse protein substrates, regulating numerous cellular and signaling processes. The enzyme palmitoylates sex steroid hormone receptors (ESR1, PGR, AR) and GNAQ to control their plasma membrane targeting and G protein-coupled receptor signaling, and also regulates cell polarity through palmitoylation of SCRIB and tight junction function via JAM3. Beyond canonical signaling, ZDHHC7 has emerged as a critical regulator of innate immunity and cell death pathways: it catalyzes NLRP3 Cys126 palmitoylation to promote inflammasome activation by enabling trans-Golgi network localization and ASC oligomerization 1, palmitoylates STAT3 to enhance T helper 17 differentiation and, when inhibited, relieves inflammatory bowel disease symptoms 2, and drives pyroptosis by palmitoylating GSDMD to direct its caspase cleavage and membrane translocation 3. ZDHHC7 also regulates autophagy through ATG16L1 palmitoylation, controlling LC3 lipidation and autophagosome formation 4. In disease contexts, ZDHHC7 dysregulation contributes to cancer progression: elevated expression correlates with poor prognosis in hepatocellular carcinoma through a DHHC7–STAT3–HIF1α positive feedback loop 5, while paradoxically ZDHHC7 loss promotes prostate cancer by increasing androgen receptor signaling 6. ZDHHC7 also drives Alzheimer's disease pathology by promoting neuronal S-palmitoylation and amyloid-β accumulation, and inhibition by 2-bromopalmitate or genetic silencing ameliorates cognitive deficits in disease models 7. ZDHHC7-mediated MAVS palmitoylation enhances antiviral innate immunity against RNA viruses 8.