Fig. 5

Proposed model of PI3K activation in CM-RES clones. a, in baseline conditions, the presence of activating KRAS mutations causes a sustained MAPK signaling independently from EGFR stimulation. b, after prolonged inhibition of the MAPK pathway through vertical suppression of EGFR and MEK, the compensatory upregulation of RTKs and their ligands generates a preferential association of RTK with PI3K