These examples from congenital diseases in which cytoplasmic actin mutations affect actin polymerization and/or interactions with ABPs, thereby altering cell morphology and/or cell migration capacity, reinforce the possibility that the ACTB and ACTG1 mutations in DLBCL and multiple myeloma can have a functional contribution to the progression of these lymphoid cancers. This evidence concerns the gene ACTB and plasma cell myeloma.