Hence the probable mechanism of the anti-tumour efficacy of DW-F5 is the down-regulation of BRAF, which leads to dephosphorylation of ERK1/2, along with the inhibition of β-catenin and Akt-NF-κB, together contributing to the inhibition of MITF-M, which in turn inhibits the anti-apoptotic molecule Bcl-2, ultimately leading to cell annihilation. The gene discussed is AKT1; the disease is neoplasm.