Cdk7, also known as cyclin-dependent kinase 7, is a key kinase. It forms the CDK-activating complex (CAK) with cyclin H and MAT1, regulating cell cycle progression via T-loop phosphorylation of cell cycle CDKs. Additionally, as a component of the general transcription factor TFIIH, Cdk7-mediated phosphorylation of RNA polymerase II at active gene promoters enables transcription. It is thus crucial for both cell cycle and transcriptional processes [1,4,5,6,7].

In multiple myeloma, Cdk7 expression positively correlates with E2F and MYC transcriptional programs. Its inhibition counteracts E2F activity, impairs MYC-regulated metabolic gene signatures, and leads to in vivo tumor regression in mouse models [2]. In small cell lung cancer, inhibiting Cdk7 with YKL-5-124 disrupts cell-cycle progression, induces DNA replication stress and genome instability, and triggers an immune-response signaling, providing a survival benefit when combined with anti-PD-1 in murine models [3].

In conclusion, Cdk7 is essential for regulating cell cycle and gene transcription. Model-based research, especially in mouse models, has revealed its role in cancers such as multiple myeloma and small cell lung cancer. These findings highlight Cdk7 as a potential therapeutic target in oncology.