To test the necessity of CRAF or MEK1/2 involved in the antitumor effect of erianin, knocking down CRAF or MEK1/2 was developed in A375 and SK-MEL-28 CDX, and the result indicated that either CRAF or MEK1/2 deficiency significantly inhibited tumor growth in A375 and SK-MEL-28, as well as reducing the efficiency of erianin in vivo (Fig. 6c–h). This evidence concerns the gene RAF1 and neoplasm.