It must also be highlighted that accurate subtyping in all patients with amyloidosis remains the key initial step, irrespective of the presence of a plasma cell dyscrasia and especially despite it, since crucially, monoclonal gammopathy plus positive amyloid biopsy does not always equal AL amyloidosis, due to significant co-occurrence with wild-type transthyretin amyloidosis.1 Authors of this comprehensive review further list the essential components that dictate achievement of best long-term outcomes for AL amyloidosis, which include the optimal utility and timing of ASCT which was first reported nearly 3 decades ago for this rare hematologic malignancy.2 Previous limited availability of effective therapies for AL amyloidosis meant that rates of stringent complete response (CR) with full normalization of serum free light chains were low. In the modern era, though, it can be argued that therapy goal is too modestconsidering the very low clonal plasma cell burden at diagnosis, the goal should perhaps be a minimal residual disease (MRD)-negative state. Rather remarkably, the first therapy for the treatment of AL amyloidosis to receive US FDA approval garnered it only quite recently.3 As such, the use of ASCT as a treatment modality in a subset of patients with AL amyloidosis who were deemed fit, and in whom the therapy would likely be safe, remained an important option.