Experimental validation confirmed solasonine suppressed SRC at both transcriptional and translational levels, and SRC overexpression significantly rescued solasonine-induced proliferative inhibition in HCC cells.<h4>Discussion</h4>These integrated findings identify SRC as a critical mechanistic node mediating the pan-cancer anti-tumor effects of solasonine, particularly in HCC, and provide a rational foundation for its further development as a multi-target therapeutic agent. The gene discussed is SRC; the disease is neoplasm.