These results highlight how tumor adaptation to the MAPK pathway blockade can occur through several mechanisms, including the following: the activation of parallel survival pathways (e.g., PI3K/AKT/mTORC1), the upregulation of RTKs such as EGFR or FGFR, and the direct reactivation of the MEK/ERK cascade through upstream genetic alterations. Here, AKT1 is linked to neoplasm.