Our results differ from the results reported in many of these studies involving both tumor and nontumor cells reporting that PI3K activation, not MAPK activation, is the principal downstream effector of HER2/HER3-signaling on cellular growth [106,108,109,110], with EGFR homodimers as well as EGFR/HER2 heterodimer complexes preferentially activating MAPK signaling and HER2/HER3 heterodimers to a lesser extent [106,111,112]. This evidence concerns the gene ERBB3 and neoplasm.