SSH3 (slingshot protein phosphatase 3) is a serine/threonine phosphatase that regulates actin cytoskeleton dynamics by dephosphorylating and activating cofilin, an actin-depolymerizing factor that promotes actin filament disassembly 1. SSH3 is expressed in multiple cell types and functions downstream of integrin-Rac1 signaling, where its activity is regulated by 14-3-3 protein binding to control cell migration and polarity 1. Beyond its canonical role in actin regulation, SSH3 has emerged as a significant oncogene in multiple cancer types. In hepatocellular carcinoma, SSH3 is upregulated in tumor tissues and promotes malignant progression by activating the FGF1-mediated FGF/FGFR signaling pathway, enhancing cell proliferation while suppressing apoptosis 2. Similarly, in pancreatic cancer, elevated SSH3 expression correlates with advanced pathological grade and staging, promoting cancer cell proliferation and migration through Notch signaling pathway activation 3. SSH3 has been identified as a potential tumor antigen in bladder urothelial carcinoma for mRNA vaccine development 4. Clinically, SSH3 represents a novel therapeutic target for cancer treatment. Additionally, SSH3 DNA methylation shows longitudinal associations with lung function and may serve as a biomarker for lung function deficit prediction 5, while SSH3 has been identified as a potential biomarker for Alzheimer's disease diagnosis 6.