A consortium from the Spanish National Cancer Research Centre (CNIO) and CIEMAT described a CRISPR‑Cas9–based approach that selectively targets tumor cells bearing amplified oncogenes. The strategy leverages oncogene overdose to induce selective lethality in cancer cells while sparing normal tissue that lacks amplification. Researchers validated the method in preclinical models and outlined gene‑editing designs that exploit copy‑number imbalances typical of certain aggressive tumors. The work aims to convert an oncogenic driver into a therapeutic liability by using targeted double‑strand breaks or CRISPR‑mediated disruption selectively in high‑copy contexts. The approach remains at an early stage; key translational issues include delivery specificity, managing on‑target toxicity in tissues with mosaic copy numbers, and regulatory pathways for in vivo gene‑editing oncology therapies.