Additionally, bufalin inhibited proliferation of Ramos cells through induction of apoptosis, activation of the caspase-3 pathways, and inhibition of the MAP kinase pathway (Fig. 7, model), suggesting that bufalin could be a main bioactive component responsible for HCS anticancer activity in aggressive B-cell lymphomas. The gene discussed is CASP3; the disease is B-cell non-Hodgkin lymphoma.