It was also found that inhibition of active MEK has different constraints downstream of oncogenic KRAS versus BRAF [130]: while KRAS-driven cancer cells are sensitive towards inhibitors interacting with MEK-Serine212 (a site critical for feedback between MEK and wildtype BRAF), BRAF-mutant cancer cells required another class of MEK inhibitor that blocks phosphorylated active MEK. Here, KRAS is linked to cancer.