NFKB1 and cancer: In agreement with DSF-Cu mechanisms of action in other cancer cell models, our studies also revealed that MPM cell growth suppression by DSF-Cu involved elevated levels of ubiquitinated cellular proteins (likely the consequence of the well-known proteasome inhibitory properties of DSF-Cu), activation of stress-activated kinases JNK1/2 and p38α/β, inhibition of NFκB signaling, and stimulation of apoptosis (Figure 9).