Yet, how CDK4/6 inhibition intersects with estrogen-regulated glycolytic control to rewire glucose utilization in ER<sup>+</sup> breast cancer has not been explored.<h4>Methods</h4>Glucose metabolism was assessed using extracellular flux analysis, untargeted metabolomics, and stable isotope tracing with uniformly labeled <sup>13</sup>C-glucose in ER + breast cancer cell lines. This evidence concerns the gene ESR1 and breast cancer.