Evolutionary studies suggest that CDK1, CDK2, CDK4, and CDK6 are critical cell cycle-related CDKs, while CDKs such as CDK7, CDK8, CDK9, and CDK11 play crucial roles in both cell cycle and transcriptional processes as transcriptional regulatory cofactors.10,11 Blocking CDK7 has been implicated in CSCs in thyroid tumors, urothelial carcinoma and pancreatic cancer by attenuating NOTCH1-cMYC, Hedgehog, or the CDK7-dependent transcriptional addictions.12–14 In addition, the CDK8-c-MYC axis has been demonstrated to govern the self-renewal potential of CSCs in glioma. Here, MYC is linked to familial pancreatic carcinoma.