Moreover, recent studies in PDAC and other cancers, suggest a considerably more complex mechanism of action for CDK4/6 inhibitors that includes multifaceted global inhibitory effects on tumour cells, stromal cells and extracellular matrix (ECM) organisation at different stages of PDAC progression [78], inhibition of epithelial-to-mesenchymal transition (EMT) signalling in breast cancer metastasis [79] and improved anti-tumour immunity by enhancing T-cell activation [80,81]. The gene discussed is CDK4; the disease is neoplasm.