FcγRIIA is a receptor for immunoglobulin G (IgG) immune complexes. FcγRIIA is expressed on human platelets over a wide range among individuals, with a median of ~4000 receptor molecules per platelet. FcγRIIA has low affinity for monomeric IgG, but strong avidity for IgG immune complexes. In addition to variation in receptor level, there is a common polymorphism in the receptor ligand binding domain, Arg131His (rs 1801274), which substantially modifies binding of IgG subclasses, notably human IgG2 and to a lesser extent IgG1. When cross-linked, FcγRIIA provides an activating signal to platelets via an immunotyrosine activation motif (ITAM) pathway. The ITAM pathway utilizes src-family kinases and Syk to produce the linker of activated T-cells (LAT) signalosome, a molecular platform involving Btk, PLCγ2, and PI3 kinase. Functional consequences include shape change, granule secretion, arachidonate metabolism, and inside-out integrin activation. When there is platelet co-stimulation by FcγRIIA and a Gq-coupled G protein-coupled receptor (GPCR) such as PAR1 and PAR4, procoagulant platelets and extracellular vesicles are generated. The principal physiological role of platelet FcγRIIA is in host defense. Platelet FcγRIIA supports clearance of circulating IgG immune complexes and IgG-coated cells, including microbes and transformed host cells. Platelet FcγRIIA supports immunothrombosis in which platelet-leukocyte transactivation combines with coagulation and inflammatory factors to minimize microbial dissemination. Over-exuberant immunothrombotic responses trigger thromboinflammation with thrombi in arteries, veins, and the microcirculation, for example, in sepsis. In disease, FcγRIIA is best known for its role in immune thrombotic thrombocytopenia syndromes, including heparin-induced thrombocytopenia (HIT) and vaccine-induced thrombotic thrombocytopenia (VITT). Additional physiological or pathological roles for platelet FcγRIIA include response to alternative ligands such as C-reactive protein (CRP), cross-regulation with collagen receptor GPVI, and enhancement of outside-in signaling via αIIbβ3. Platelet FcγRIIA is under active investigation as a key mediator of microbial infection, systemic autoimmune diseases, cancer metastasis, and cardiovascular disease, among others. There is ongoing progress in the use of platelet FcγRIIA as a biomarker and a target for novel therapeutics.