In Science Signaling this week, researchers in the UK say amplification of oncogenes KRAS or BRAF underpins an acquired resistance to MEK1/2 inhibitors in colorectal cancer cells. The researchers modeled acquired resistance to the MEK 1/2 inhibitor selumetinib in colorectal cancer cells with BRAF or KRAS mutations. Genomic sequencing showed no acquired mutations in MEK1 or MEK2, selumetinib's primary targets.