Unexpectedly, we also observed that stable overexpression of inhibitor kappa kinase beta (IKKβ), which normally functions to phosphorylate IκBα in the cytoplasm, allowing for activation of NFκB-mediated signaling, significantly decreases SIM2s gene expression in the DCIS.COM cells suggesting a reciprocal relationship between NFκB and SIM2s (Fig. 2a). This evidence concerns the gene NFKBIA and ductal breast carcinoma in situ.