As we have previously demonstrated that pharmacologic inhibition of PKC activity by using CC resulted in abrogation of TSA-mediated NF-κB activation and enhancement of apoptosis in cells treated with the TSA+CC combination (Maxhimer et al, 2005), we sought to determine if STP or UCN-01, via being PKC inhibitors as indicated by their ability to markedly reduce the expression of phosphorylated α/γ adducin (p-adducin) (Figure 1A), could duplicate the effect of CC in suppressing NF-κB activation and enhancing the cytotoxic effect of TSA in cultured thoracic cancer cells. The gene discussed is CXCR1; the disease is thoracic cancer.