A possible example is the TEAD1 gene, which is known to be over-expressed in aggressive and treatment-refractory cases of multiple myeloma [51] and which showed de novo ASM in its upstream enhancer region in a multiple myeloma case in our series, via gain of a new TF binding motif on the mutated allele (Fig. 5). The gene discussed is TEAD1; the disease is AL amyloidosis.