Platelet receptor Gi24, also known as Dies1, VISTA, SISP1 and B7‑H5, is a 55‑65 kDa transmembrane glycoprotein with homology to B7‑like immune co‑stimulatory molecules (1, 2). Mature human Gi24 contains a 162 amino acid (aa) extracellular domain (ECD) with one V‑type Ig‑like domain, a 21 aa transmembrane segment, and a 96 aa cytoplasmic domain. Within the ECD, human Gi24 shares 70% and 67% aa sequence identity with mouse and rat Gi24, respectively (3). The 30 kDa ECD can be shed by MT1‑MMP, with a 25‑30 kDa fragment remaining in the membrane (3). Gi24 promotes both MT1‑MMP expression and the MT1‑MMP mediated activation of MMP‑2 (3). Gi24 supports the differentiation of embryonic stem cells (ESC) and enhances BMP‑4 induced signaling in ESC, but is also down‑regulated following BMP‑4 exposure (4, 5). It binds to BMP‑4 directly, and also associates with the type I BMP receptor Activin RIB/ALK‑4 (4, 5). Gi24 is expressed on the surface of naïve CD4 ⁺ T cells and regulatory T cells (6). It is up‑regulated in vivo on activated monocytes and dendritic cells (5). Gi24 inhibits CD4 ⁺ and CD8 ⁺ T cell proliferation, and their production of IL‑2 and IFN‑ gamma (6). Its expression on tumor cells attenuates the anti‑tumor immune response and enables more rapid tumor progression (6). In contrast, Gi24 limits disease progression in the autoimmune disease model EAE (6).