Specifically, we observed that CUMS-induced depression models exhibited profound molecular dysregulation characterized by significant BDNF suppression (Fig. 4E), pathological EGFR overexpression (Fig. 4F), ERK2 downregulation (Fig. 4G), pro-inflammatory JUN elevation (Fig. 4H), RAF1 repression (Fig. 4I), and chronic stress-driven TNF upregulation (Fig. 4J). This evidence concerns the gene EGFR and depressive symptom measurement.