We examined the phosphorylation levels of MEK1/2 and ERK1/2 in BRAF-mutant, KRAS-mutant, or EGFR-mutant cancer cell lines after RAF inhibitor treatment to investigate the correlations between the dimerization potencies of the RAF inhibitors and their abilities to induce paradoxical activation of MEK-ERK signalling. Here, MAPK3 is linked to cancer.