The study by Tamaki et al. showed that activation of GPER through G-1 (a specific agonist) on human eosinophils inhibits the enzymatic activity of caspase-3 and reduces spontaneous apoptosis, suggesting a potential mechanism for GPER's impact on asthma pathogenesis; thus, these findings prove a mechanism of direct interaction between estrogen and eosinophil functions (70). The gene discussed is GPER1; the disease is asthma.