Knockdown of XBP1 in BMSCs compromises BMSC secretion of RANKL and support of OCL formation. (A) Western blot demonstrating the effects of XBP1 knockdown on the baseline and TNFα-induced sRANKL protein levels in the total lysates of the BMSCs of both healthy donors (n = 3; left) and MM patients (n = 4; right). β-actin served as the loading control. (B) Schematic quantitative representation of results shown in panel A. The sRANKL protein levels were normalized to those of β-actin. The baseline relative sRANKL protein levels of the healthy donor BMSCs in the absence of hXbp1 shRNAs are arbitrarily defined as 1. Error bars represent means ± SD. (C) Effect of XBP1 knockdown on the capacity of MM patient BMSCs to support OCL formation (n = 3; mean ± SD; *P < .05).