CHN2 encodes β-chimaerin proteins (β1, β2, and β3 isoforms), which function as GTPase-activating proteins (GAPs) specifically targeting Rac 1. These proteins contain characteristic SH2, C1, and Rac-GAP domains and are responsive to diacylglycerol and phorbol esters 1. CHN2 plays important roles in insulin signaling, as demonstrated by a case where CHN2 haploinsufficiency combined with INSR disruption resulted in severe insulin resistance and growth deficiency, with CHN2 being expressed in insulin-sensitive tissues 2. The gene also contributes to disease susceptibility, with genetic variants associated with diabetic retinopathy in Chinese type 2 diabetic patients 3 and smoking behavior 4. CHN2 expression is regulated by environmental factors, as prenatal phthalate exposure affects DNA methylation patterns near CHN2 5. Additionally, CHN2 expression is altered in systemic lupus erythematosus, being downregulated in neutrophils from adult SLE patients 6. The multiple CHN2 isoforms arise from alternative transcription start sites rather than splicing, with β3-chimaerin showing enhanced phorbol ester responsiveness compared to β2-chimaerin 1.