As the HER2+ lines we studied are less sensitive to the interruption of RALA and RALB signaling, we hypothesize that their tumor phenotypes are instead driven by a distinct pathway that may exist downstream of RAS, such as RAF/MEK/ERK, or be wholly independent of RAS signaling, such as the PI3K/AKT/MTOR pathway downstream of HER2/HER3 heterodimerization. The gene discussed is MTOR; the disease is neoplasm.