The “cell cycle” vs. “immune” tumor subtype was indeed a significant determinant of responsiveness to vemurafenib as published (hazard ratio (HR) = 2.15; P = 0.0085; Fig. 3a).37 However, BRAF-mutant tumors with higher MPAS (and therefore higher MAPK pathway signaling) did significantly better than those with low MPAS across all patients on vemurafenib (HR = 0.596; P = 0.018; Fig. 3a, b). The gene discussed is BRAF; the disease is neoplasm.