This study included a small group of patients with uveal melanoma with no clinical and laboratory evidence of infection who were treated with the therapeutic antibody tebentafusp, a bispecific antibody that docks T cells to glycoprotein 100 (gp100) on melanoma cells and induces the release of several inflammatory cytokines [49] to explore the activity of cytokines on the PMN and MO surface markers we explored here. The gene discussed is PMEL; the disease is melanoma.