Together with the normal levels of ERK phosphorylation observed in all RAF1 KO CRC cell lines/PDO and with the rescue of the RAF1 phenotype by a kinase-dead mutant (functional as an activator) the data indicate that the role of RAF1 in CRC is independent of its kinase activity, and that the role of the RAF1 dimerization interface is unlikely to be rooted in its effect on the ERK pathway. Here, MAPK1 is linked to colorectal carcinoma.