Finally, the anticancer CuB mechanism is not limited to JAK/STAT pathway disruption but also induces disruption of many other types of signaling that increase tumor cell growth, such as NFκB [68], PI3K/Akt/mTOR [44], MAPK/ERK [65], or Wnt/β-catenin progression [69]. This evidence concerns the gene NFKB1 and neoplasm.