Most frequently mutations were found in NRAS, KRAS, FAM46C, TP53, BRAF, NFKB1, CYLD, LTB, IRF4 and CCND1. 13, 14, 15, 16 Many of these mutations are conceived as driver mutations, some of which potentially druggable, at least if present in more than a tumor subclone, and others have prognostic relevance.17, 18, 19, 20, 21, 22, 23 It is therefore vital to develop clinically utilizable tools that may help to quickly generate a picture of the clonal architecture of a given patient with a plasma cell disorder. This evidence concerns the gene TP53 and plasma cell neoplasm.