From a therapeutic perspective, the development of next-generation transthyretin stabilizers, gene-silencing agents, and gene-editing technologies holds considerable promise for transforming the management of ATTR amyloidosis [60,61,62], whereas targeted immunotherapeutic strategies aimed at neutralizing circulating amyloidogenic light chains or facilitating fibril clearance may substantially improve clinical outcomes in AL amyloidosis [62,63]. The gene discussed is TTR; the disease is AL amyloidosis.