The cyclin-dependent kinase (CDK) family comprises one of the most common types of serine/threonine kinases responsible for controlling many cellular processes through the action of the dynamics of these enzymes. The CDKs are regulators of cellular processes, ranging from cell cycle progression, an integral step of cellular lifespan involved in its division and growth, to the expression of genes and the transfer of genetic information from DNA to RNA. CDK-related pathology is primarily based on the dysregulation of CDK, resulting in improper coordination of the cell cycle and leading to uncontrolled proliferation. The CDK1 involved in the G2 to M-phase transition interacts with CENPF, PVT1, and TFCP2L1, which affects chromosome segregation and cell proliferation. Besides the previously described partners, namely PRDX2 and C/EBPα, the CDK2 responsible for the G1/S transition has also been shown to bind TBK1 and modulate DNA synthesis and cell cycle checkpoints. Such mechanisms of action contribute to oncogenesis through interactions, including roles for lncRNAs and miRNAs in modulating the expression and activity of CDKs. Their importance in cancer has made CDK1/2 critical candidates for anticancer drug targeting. The dysregulation of CDK1/2 manifests in cancer pathology, which is, in turn, associated with an uncoordinated normal cell cycle and resultant proliferation. This study aims to provide a comprehensive overview of the diverse functions of CDK1 and CDK2 in cancer, thereby facilitating the exploration of their therapeutic potential and the development of novel cancer therapy designs. The complexity of targeting CDK1 and CDK2 highlights the importance of their regulation during cancer development. It indicates their substantial promise as valid targets for therapy, in vitro and vivo studies, and human sample analysis.