RGS2 (regulator of G protein signaling 2) is a negative regulator of G protein-coupled receptor (GPCR) signaling that functions by increasing GTPase activity of G protein alpha subunits, driving them into their inactive GDP-bound form 1. The protein plays critical roles in cardiovascular regulation, with ZFP36-mediated destabilization of RGS2 mRNA leading to increased vascular smooth muscle contraction and elevated blood pressure 2. In immune contexts, RGS2 demonstrates complex regulatory functions. It can inhibit PD-L1 translation when coordinating with lncRNA HITT, thereby enhancing T cell-mediated cytotoxicity 3. However, RGS2 is also highly expressed in exhausted CD8+ T cells and is transcriptionally regulated by BATF2, where it promotes T cell exhaustion and tumor immune evasion by inhibiting CXCL13 secretion 4. Additionally, RGS2 shows differential expression patterns in neuropsychiatric conditions, being up-regulated in Brodmann Area 10 samples from schizophrenia patients 5. The protein's involvement extends to tissue repair functions, as it is among genes upregulated during macrophage activation by plasma extracellular vesicles, promoting anti-inflammatory responses and tissue remodeling 6. These diverse functions establish RGS2 as a crucial regulator across cardiovascular, immune, and neurological systems.