Systemic amyloidosis is a group of disorders marked by the extracellular deposition of misfolded proteins forming amyloid fibrils, which accumulate in organs and cause dysfunction. In AL amyloidosis, the amyloidogenic proteins are immunoglobulin light chains produced by clonal plasma cells. AL amyloidosis often arises in the context of plasma cell disorders, including monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM), although it can occasionally emerge from other B-cell disorders. Clinical manifestations vary by organ involvement, with major impacts on the heart, kidneys, nervous system, and gastrointestinal tract. Diagnostic strategies include detecting monoclonal proteins through serum electrophoresis, immunofixation, and free light chain assays, while tissue biopsies with Congo red staining confirm amyloid deposition. In particular, amyloid fibril typing is essential to distinguish AL amyloidosis from other types, such as transthyretin amyloidosis. Recent treatment advances have improved outcomes; standard therapy now includes daratumumab with bortezomib, cyclophosphamide, and dexamethasone. This regimen has shown efficacy in reducing plasma cell burden and improving survival rates. Emerging therapies, including anti-amyloid antibodies and BCMA-targeted treatments, offer promising results. The revised Mayo Clinic Amyloid Staging system now incorporates amyloidogenic FLC levels to better predict long-term outcomes based on organ progression. With advances in early diagnosis and innovative therapies, the prognosis in AL amyloidosis has improved, but early intervention remains critical to prevent irreversible organ damage and improve patient survival.