Having established the importance of the CDK2-associated kinase activity in aberrant acinar morphogenesis in 3D culture and given that the b-Raf-ERK1/2-mTOR signaling axis was deregulated in tumor cells and patient samples with high LMW-E expression, we hypothesized that combination treatment with roscovitine (a CDK inhibitor) plus either rapamycin (an mTOR inhibitor) or sorafenib (a pan kinase inhibitor that has activity against b-Raf) can prevent the induced-aberrant acinar morphology. The gene discussed is MTOR; the disease is neoplasm.