In several preclinical models, we have observed enhanced TEAD activity and target gene transcription after treatment with MAPK-related inhibitors, including in BRAFV600E CRC and in KRAS-mutant PDAC, consistent with a compensatory adaptation mechanism to MAPK blockade that could increase susceptibility to YAP/TEAD inhibition. Here, YAP1 is linked to colorectal carcinoma.