While cancer cells often overexpress death receptors DR4 and DR5, healthy cells often overexpress the decoy receptors DcR1 and DcR2 as a mechanism to prevent undesired apoptosis.31, 32 However, studies have shown that one mechanism of resistance to TRAIL is to decrease death domain activation by either downregulating or mutating DR4/DR5 or upregulating the protective DcR1/DcR2 receptors.33 Western blot analysis showed that H446 cells indeed did express high levels of both death receptors and no detectable levels of the decoys, explaining their responsiveness to TRAIL treatment. Here, TNFRSF10B is linked to cancer.