CRBN and AL amyloidosis: Targeting CRBN by IMiDs modifies its substrate specificity towards non-physiological proteins which are subsequently ubiquitinated and degraded by the proteasome [4,5,6,7,8,9,10], Figure 1A. This mechanism of action has shown particular relevance in the treatment of multiple myeloma (MM), the second most common hematological malignancy with a recurrent clinical course leading to 20,000 deaths per year in the European Union [11].