Bone disease in multiple myeloma (MM) is characterized by increased bone resorption and impaired osteoblast activity, resulting in lytic bone lesions. 1 Therefore, the biochemical markers of osteoblastic activity seem not elevated in most cases of MM. Recently, bortezomib, a proteasome inhibitor, has been shown to have an antimyeloma activity by blocking nuclear factor-кB (NF-кB)-mediated IL-6 production from bone marrow (BM) microenvironment, and inducing apoptosis of myeloma cells. 2 It acts in the BM microenvironment to inhibit the binding of myeloma cells to BM stromal cells, the transcription and secretion of IL-6 triggered by myeloma cells to BM stromal cell adhesion, and BM angiogenesis. Phase II trial of bortezomib in patients with refractory MM demonstrated the overall response rate of 35%, with 10% of patients being in complete response (CR). 3 However, the effect of bortezomib on bone lesions remains unknown. We here report a patient with MM who showed the high serum total alkaline phosphatase (ALP) as well as bone-specific alkaline phosphatase (BAP) levels after bortezomib-combined therapy, which suggests that bortezomib induced osteoblastic differentiation.