Previous investigations demonstrated the indispensable role of RIPK3 in cell death regulation during embryonic development,54, 55, 56 stimulation with different ligands of the TNF superfamily,5, 57 TLR3 agonists,4, 58 during etoposide-mediated stress responses9 and on interferon signalling or during virus infections.7, 59, 60 In our study, reconstitution of RIPK3 not only increased apoptosis as recently reported8, 24 but also allowed reactivation of necroptosis in melanoma whenever IAPs are inhibited. The gene discussed is TLR3; the disease is melanoma.