ATCC and the Broad Institute reported engineered isogenic NSCLC models designed to replicate resistance mechanisms that emerge during EGFR-mutant treatment with osimertinib. The platform uses CRISPR gene editing and gene overexpression to generate drug-sensitive and drug-resistant cell lines side-by-side. The report frames the work as a response to the slow and sample-limited nature of patient-derived longitudinal modeling, proposing that lab-engineered resistance pathways can accelerate discovery of combination therapies. Lead researchers highlighted the use of CRISPR and overexpression to cover representative resistance mechanism classes to osimertinib. The stated goal is to reveal hidden targets and combination strategies that turn current treatment failures into next-generation breakthroughs. ATCC and Broad said they plan to provide these models and associated data to the research community. For drug developers, the practical value is faster preclinical resistance modeling that can support hypothesis testing and better-informed target selection.