Interestingly, recurrent genetic aberrations drive the overexpression of NSD2 in multiple myeloma and pediatric leukemia, and of NSD2, NSD3 and SETDB1 in lung cancer [41], [42], [43], [44], which could possibly offer an opportunity for targeted protein methylation in cells presenting a specific disease-associated genetic profile. Here, SETDB1 is linked to AL amyloidosis.