AKT1 and cancer: Thus, treatment of MCF‐7 or SK‐BR‐3 breast cancer cells with the CDK4/6 inhibitor PD0332991 also caused an upregulation of MYC, GLS1 and the mTOR and Akt signaling pathways, as well as a downregulation of HIF‐1α (Fig 5J), suggesting that upregulation of MYC, with its consequent downstream effects, is an adaptive response to CDK4/6 loss of function conserved among several types of cancer cells.