Our demonstration of B2M mutations and LOH only in progression samples in our cohort (several CPB therapies, n = 17 patients, 49 longitudinal samples) as well as enrichment of B2M LOH in non-responders with poorer overall survival in two independent cohorts (anti-CTLA4, n = 105; anti-PD1, n = 38), suggests that B2M-mutated tumor subclones are selected through immunoediting earlier in tumor development, or under selective pressure applied by CPB. The gene discussed is B2M; the disease is neoplasm.