Researchers at Spain’s CNIO and CIEMAT described a gene‑editing approach that selectively targets tumors with oncogene amplifications using CRISPR‑Cas9 vulnerabilities tied to genomic overload. The method exploits the tumor’s amplified loci to induce lethal DNA damage selectively in cancer cells with high oncogene copy number. Preclinical data showed selective tumor cell killing while sparing normal tissues lacking the amplifications, positioning the approach as a potential precision therapy for tumors defined by copy‑number gains rather than single driver mutations. The team emphasized validating off‑target effects and delivery mechanisms as next steps. If delivery and safety hurdles can be overcome, the technique could expand CRISPR’s therapeutic niche to cancers driven by gene amplification, offering a distinct complementary strategy to small molecules and biologics.