In MCF-7 cells, some may think that inhibition of Akt would be the main mechanism for boosting CDDP efficacy because AIMs clearly inhibited the activation of Akt that was induced by CDDP (Figure 4) and that Akt regulates NF-κB by suppressing IκB degradation and also promotes cancer cell survival by activating anti-apoptotic proteins and inactivating pro-apoptotic proteins [34]. The gene discussed is PROS1; the disease is cancer.