A high tumor mutation burden (TMB) is associated with the efficacy of ICIs that target neoantigens derived from somatic variants.5 Malignant melanoma is characterized by a high TMB resulting from the accumulation of sun exposure–derived DNA damage, which, in turn, endows it with sensitivity to ICIs.6 Alternatively, the BRAF V600E and V600K variants are additional actionable genomic biomarkers that predict responses to BRAF/MEK inhibitors. The gene discussed is BRAF; the disease is neoplasm.