Mechanistic studies demonstrate that the inhibition of NSCLC proliferation by lunasin is the result of a combination of alterations in the expression of the cyclin-dependent kinase (CDK) complex components cyclin D1, CDK4 and CDK6 and the timing of Akt activation by phosphorylation at S473, which acts as a negative regulator of p27Kip1 expression. The gene discussed is CCND1; the disease is non-small cell lung carcinoma.