In this article, we highlight emerging evidence supporting the proposition that the signaling pathways anchored by Basigin/CD147 and CD36, two of the known host receptors that control Pf invasion and cyto-adherence, respectively, are also targets for functional subversion by Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV), an inherently persistent cancer-associated herpesvirus that is prevalent in malaria-endemic regions. The gene discussed is BSG; the disease is cancer.