(5) Studies with a panel of lung cancer cell lines showed that morusin treatment not only modulates conventional targets including NF-κB, STAT3 and downstream genes such as VEGF but may also directly bind and dephosphorylate EGFR on an active site, which would contribute to the further reduction of STAT3/NF-κB activity [14]. This evidence concerns the gene NFKB1 and lung carcinoma.