Due to its mode of action, i.e., operating downstream of NF-κB, DTP3 bypassed resistance to multiple drugs used in MM (i.e., steroids, immunomodulatory drugs, proteasome inhibitors), creating a unique profile of clinical utility for development in MM and DLBCL [229,234,235]. This evidence concerns the gene NFKB1 and diffuse large B-cell lymphoma.