CSRP2 is a cysteine and glycine-rich LIM domain protein located on chromosome 12.1 1 that functions as a multifaceted oncogenic regulator across diverse cancer types. Originally characterized as drastically downregulated during smooth muscle cell dedifferentiation, CSRP2 is now recognized as significantly upregulated in glioblastoma, neuroblastoma, hepatocellular carcinoma, B-cell acute lymphocytic leukemia, and head and neck squamous cell carcinoma, correlating with poor prognosis 23456. Mechanistically, CSRP2 promotes cancer progression through multiple pathways: it activates p130Cas-mediated NF-κB and MAPK signaling in glioblastoma 2, drives ERK1/2 phosphorylation in neuroblastoma 3, regulates ATF2-mediated CCL28 expression to reshape immunosuppressive tumor microenvironments in hepatocellular carcinoma 4, and activates JAK-STAT1 pathways in glioma to inhibit necroptosis 7. CSRP2 also promotes epithelial-to-mesenchymal transition, cancer stemness, and chemotherapy resistance. Beyond malignancy, CSRP2 upregulation contributes to pulmonary hypertension through Wnt3α-β-catenin/LEF1 pathway activation, driving vascular smooth muscle cell proliferation 8. These findings establish CSRP2 as a critical therapeutic target across multiple disease contexts.