Disruption of the allosteric activating function within the HER3 KD C-lobe or disrupting the AP-2 helix binding activity of the HER3 KD N-lobe substantially impairs tumor growth (Figure 4B), confirming the essential role of these functions in tumorigenic signaling and the potential of these sites as targets for novel classes of pharmaceutical agents. Here, ERBB3 is linked to neoplasm.