Inhibition mechanism of BMS-345541 and Purvalanol A in HTLV-1 infected cells results in blocking canonical NF-κB signaling pathway and cell cycle progression. In the absence of drug, hyperactive IKK complex phosphorylates IκB-α resulting in IκB-α degradation and p65/p50 translocation. The genes transcribed by p65/50 include anti-apoptotic genes which are responsible for survival of virus infected cells. In the presence of BMS-345541, the activity of IKK complex is inhibited which results in decreased IκB-α phosphorylation, therefore p65/p50 are kept in cytoplasm. Hence, the expression of anti-apoptotic proteins are decreased which make HTLV-1 infected cells more susceptible and sensitive to the action of the drug. Without drugs, cyclin E/CDK2 phosphorylates Rb and induces Rb degradation. The free E2F then transcribes genes which are necessary for G1/S transition. However, Purvalanol A inhibits CDK2 (a non-essential protein in the life cycle of a cell) activity, as previously shown by us, which results in decreased Rb phsophorylation and inactivated E2F. Therefore, the infected cells may be blocked at the G1 checkpoint and simultaneously have lower viral expression.