Although limited to the exome (2% of the whole genome), the mutational analysis of primary tumor samples has yielded a better understanding of the clonal evolution of myeloma, including difficult questions such as whether mutations that target the same pathway (e.g., KRAS-, NRAS-, or BRAF-dependent activation of MAPK signaling) occur in the same cell clone or are distributed among different cell clones admixed in the same diagnostic bone marrow sample (Bolli et al., 2014). The gene discussed is BRAF; the disease is plasma cell myeloma.