As tumor suppressors and activated oncogenes also contribute to drug and radiation resistance [26,27,28], we also tested whether mutations in the tumor suppressor gene TP53 or the H-RAS, K–RAS, and N-RAS genes as well as the mRNA expression of the epidermal growth factor receptor gene (EGFR) are associated with cellular response to scopoletin. Here, KRAS is linked to neoplasm.