CCND1 encodes cyclin D1, a regulatory protein that forms a complex with CDK4 to phosphorylate and inactivate retinoblastoma (RB) protein family members during the G1/S transition of the cell cycle. By phosphorylating RB1, cyclin D1-CDK4 releases the transcription factor E2F, allowing transcription of genes required for G1 phase progression. Cyclin D1 also acts as a transcriptional corepressor with INSM1 in a cell-cycle-independent manner and integrates mitogenic and antimitogenic signals. CCND1 amplification or overexpression drives multiple cancer types. In mantle cell lymphoma, constitutive cyclin D1 overexpression results from t(11;14)(CCND1;IGH) translocation; in multiple myeloma with this translocation, RAS pathway mutations confer resistance to the BCL2 inhibitor venetoclax 1. In metastatic breast cancer, CCND1 amplification is associated with shortened progression-free survival in patients receiving aromatase inhibitors (16.0 vs. 32.4 months) 2. In gastric cancer, elevated CCND1 levels—enhanced by circNFATC3-stabilized IGF2BP3 3 or GABRD-mediated suppression of ubiquitin degradation 4—promote proliferation and poor survival. CCND1 copy number gains also occur in acral melanoma 5. Clinically, palbociclib, a CDK4/6 inhibitor, targets cyclin D1-CDK4 complexes in cancer treatment. These findings establish CCND1 as a critical driver of oncogenic cell cycle progression across multiple tumor types.