Light chain (AL) amyloidosis is caused by misfolded light chains depositing in tissues in the form of fibrils, leading to organ damage [1]. Treatment consists of plasma- cell directed therapy to halt the production of the toxic light chains. There is currently a dynamic clinical research landscape with the recent develop- ment of several promising therapies. While phase 1 trials focus on safety, phase 2 and 3 trials provide essential efficacy data[2], with hematologic response representing a well- established effi- cacy endpoint in AL amyloidosis. Measurable disease is required to ensure that the hematologic response can be adequately as- sessed. M- protein based hematologic response criteria have remained unchanged since 20 05 (Table1) [3]. Hematologic re- sponse criteria based on the difference between the involved and uninvolved free light chains (dFLC) were updated in 2012
