In patients progressing following CKI treatment, the vast majority of whom would eventually die from metastatic melanoma, we have cautiously added low doses of targeted agents when a druggable mutation was present (e.g., BRAF with or without MEK inhibitors) with the hypothesis that these agents would slow cancer growth to provide time for productive immune responses to develop and perhaps to take advantage of mmune potentiation induced by BRAF±MEK inhibitors [23–26]. The gene discussed is CHKA; the disease is cancer.