CDC7 (cell division cycle 7) is a serine/threonine kinase essential for DNA replication initiation, functioning through phosphorylation of MCM proteins and other critical substrates during the G1/S phase transition 1. The kinase forms a complex with its regulatory subunit ASK/Dbf4 (DDK complex) to promote origin firing and fork restart by phosphorylating substrates including MERIT40 and PDS5B 2. Beyond replication initiation, CDC7 regulates DNA repair, recombination, and replication stress responses through coordination with ATR-Chk1 signaling and the RAD18-dependent DNA damage bypass pathway 3. Clinically, CDC7 represents a druggable vulnerability in multiple cancer types. CDC7 inhibition induces senescence in TP53-mutant hepatocellular carcinoma, which becomes lethal when combined with mTOR pathway inhibition 4. In ovarian cancer, CDC7 inhibitors synergize with PARP inhibitors by increasing DNA replication stress and triggering cGAS/STING-mediated antitumor immunity 5. CDC7 inhibition also suppresses neuroendocrine transformation in lung and prostate cancers through MYC degradation, preventing therapy resistance 6. These findings establish CDC7 as both a biomarker of cancer cell dependencies and a promising therapeutic target across multiple malignancies 7.