BRAF mutations that result in constitutive cell proliferation are present in roughly 50% of malignant melanoma.35 The BRAF inhibitors Vemurafenib or Dabrafenib suppress proliferation of BRAF-mutated melanoma cells,36 but surprisingly Dabrafenib effectively suppresses RIPK3 activity as an off-target effect.37 Thus, it is intriguing to speculate that the effectiveness of a therapy with BRAF inhibitors could be hampered (or altered) by interference with necroptosis/RIPK3 signalling. The gene discussed is BRAF; the disease is melanoma.