Since this master regulator has been implicated in tumor development and progression [44, 45], we next investigated if NFkB contributes to CSC-mediated activation of ZFAS1. qRT-PCR assays revealed that endogenous NFkB-p65 mRNA levels were higher in lung cancer cells relative to NREC; similar to what we observed for SP1, 5-day CSC exposure did not upregulate NFkB-p65 expression (Fig. 11A). The gene discussed is NFKB1; the disease is lung carcinoma.