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In the presence of BRAF V600E inhibition (large red X), the BRAF/KRAS mutant cells, KTC1-VEM2, are able to drive activation of survival and proliferation pathways (PI3K/AKT and RAF/MEK/ERK) through the KRAS G12D mutation and increased RTK (EGFR and HER3) activation. The KRAS G12D mutation is insensitive to the actions of GTPase-activating proteins (small red X) and is constitutively active (orange asterisk).
