While physiological STAT3 activation is transient, rapidly returning to the basal state, STAT3 becomes inappropriately and persistently activated in a wide variety of hematopoietic and solid malignancies, including melanoma, multiple myeloma, breast, prostate, ovarian, and colon cancer [4], due to upregulation of upstream signaling pathways attributed to molecules that are produced within the tumor microenvironment [5]. This evidence concerns the gene STAT3 and AL amyloidosis.