Moreover, inhibition of the immuno/proteasome’s function by carfilzomib also affects additional pathways, including the apoptosis, autophagy, and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) pathways, as well instigating the unfolded protein response (UPR); this may explain the marked reduction in cell density and the slowing of tumor growth, since this response pathway in particular culminates in apoptosis when homeostasis is not restored due to carfilzomib’s activity [44,45,46]. Here, NFKB1 is linked to neoplasm.