We thank Yu et al for their interest in our recent work on the evolution of esophageal adenocarcinoma (EAC).1 They highlight the potential of our stem cell cloning approach to illuminate key steps in EAC development and to serve as a platform for risk stratification and therapeutic strategies across successive precursor lesions. However, they express concerns for one of our conclusions, which appears to challenge the long-held view that EAC and other solid tumors are characterized by intrinsic genomic instability.
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