Growth and survival of B-Raf(V600E) cancers is driven by B-Raf(V600E)-activated MAPK, as well as by a variety of de-repressed RTKs and transduction pathways that resist B-Raf(V600E) kinase inhibitors, including ErbB members, IGF1R, c-Met, IRS/PI3K/Akt/mTORC1, C-Raf/MEK/MAPK, Jak/STAT3 and/or c-Src [7–15]. This evidence concerns the gene STAT3 and cancer.