In contrast to previous findings, a role for RUNX2 in alleviating drug resistance was reported: in multiple myeloma, a mouse model with specific RUNX2 deficiency in osteoblasts (RUNX2−/−) rendered multiple myeloma cells more resistant to bortezomib via thrombospondin-1-mediated TGFβ1 activation, whereas the malignancy and tumor burden were reversed by treatment with the antagonist SRI31277 [41]. This evidence concerns the gene TGFB1 and AL amyloidosis.