Unlike these previous studies, our goal was not to prevent SHP2 adaptive resistance to inhibition of MEK/ERK signaling but rather to exploit SHP2 regulation of parallel pathways (e.g., AKT, JAK/STAT) that control the production of vascular regulators, cell adhesion, and cell survival, prompting a change of the tumor architecture to segregate tumor cells into vascular islands. This evidence concerns the gene AKT1 and neoplasm.