These include (1) direct HDL mediated survival signaling in cardiomyocytes leading to protection against cytotoxicity, as exemplified by studies using DOX as a cardiotoxic agent; (2) indirect protection afforded to the heart by utilizing rHDL-based nanoparticles as targeted delivery vehicles for chemotherapeutic agents which spare the heart and have the potential to target tumor cells which may overexpress SR-B1; and (3) indirect protection resulting from direct ApoA1 mediated tumor suppression (Figure 4). The gene discussed is SCARB1; the disease is neoplasm.