The FDA approval of camizestrant (Etcamah) is expected to enable ctDNA-guided switching in advanced estrogen receptor–positive, HER2-negative breast cancer as resistance emerges through ESR1 mutations. The approval positions clinicians to move earlier once ESR1 alterations surface in circulating tumor DNA rather than waiting for clinical progression. In an interview, Erica L. Mayer of Dana-Farber Cancer Institute highlighted that a regimen using early camizestrant switching combined with a CDK4/6 inhibitor after an ESR1 mutation appears in ctDNA improved progression-free survival and delayed quality-of-life deterioration compared with continuing an aromatase inhibitor strategy. Mayer described camizestrant as an oral selective estrogen receptor degrader and emphasized the approval’s broader significance: integrating molecular monitoring into treatment decisions for ESR1 resistance. The key operational change is the shift from imaging-and-symptoms-driven switching to biomarker-driven intervention, which can affect trial designs, testing workflows, and how sponsors plan future resistance strategies.