A 56-year-old male with no comorbidities presented with a 1-year history of progressive, asymmetric bilateral shoulder weakness. Examination was notable for moderate-to-severe asymmetric weakness and atrophy of shoulder girdle muscles, right worse than left. EMG demonstrated a proximal, axial myopathy with fibrillation potentials.  CK was elevated at 439 U/L (N<308). Monoclonal gammopathy screen showed a small IgG lambda monoclonal gammopathy with elevated lambda free light chain at 20.7 mg/dl (N: 0.57-2.63) with K/L ratio of 0.0787 (N: 0.26-1.65). A right triceps muscle biopsy demonstrated AL lambda amyloid myopathy. Mass-spectrometry–based proteomics identified an AL lambda peptide profile. Fat aspirate mass-spectrometry identified AL lambda and AA (serum amyloid A) peptide profiles. A subsequent abdominal fat pad biopsy demonstrated again both AL and AA amyloid deposits. Bone marrow biopsy showed 5% lambda light chain restricted plasma cells, and AL and wild-type ATTR periosteal amyloid deposits. The same amyloidogenic light chain variable region belonging to family LV1-47/LV1-44 was identified in all three sites. TTR gene sequencing was negative. Major organ involvement was ruled out by laboratory tests, as well as PYP-SPECT-CT.  The patient was started on daratumumab, bortezomib, cyclophosphamide and dexamethasone. On follow up, she achieved complete hematological response and partial clinical improvement.