Fig. 2

a MM Expressing Active RKIP. Blue arrows signify the interactions of gene products. Black arrows signify whether the expression of the associated gene product is increased or decreased. If RKIP expression is assumed to be high and functional, then high DR5 expression would be expected through the action of NF-κB inhibiting YY1 [14]. PTEN is expected to be highly expressed through the action of NF-κB inhibiting YY1, which will no longer inhibit PTEN, thus causing PTEN overexpression [13]. Bcl-2 is overexpressed in the data, but according to findings in literature, if RKIP is overexpressed, Bcl-2 should be inhibited via NF-κB and PTEN [61, 69]. In the outlined pathway, Fas is expected to be overexpressed, but in the data, Fas is overexpressed in MM [13]. No clear relationship is determined with RKIP overexpression and Bcl-6, TNFR-2, TRAIL, and TNF-α. b MM Expressing Inactive, Phosphorylated RKIP. Blue arrows signify the interactions of gene products. Black arrows signify whether the expression of the associated gene product is increased or decreased. In multiple myeloma, high RKIP expression often corresponds to phosphorylated RKIP, which is inactive [11]. Inactive (“low” or phosphorylated RKIP) would correspond to TNF-α overexpression via the expression of NF-κB, since inactive RKIP may not be able to inhibit NF-κB [70]. This would also correspond to underexpression of Fas via NF-κB's activation of YY1, which would inhibit Fas [13]. The overexpression of Bcl-2 would be explained via the inactivation of PTEN via YY1 expression and the activation of Bcl-2 with NF-κB [61, 69] However, in the data, PTEN and DR5 are overexpressed and Bcl-6 is underexpressed, which is opposite to their expected expression found literature findings [13, 62]. There is no clear relationship between RKIP inactivation and TNFR-2 and TRAIL levels