It has become clear that BRAF inhibition in colon cancer can lead to activation of EGFR through an ERK-dependent negative feedback loop and induce further upregulation of other receptor tyrosine kinases, including the other human epidermal growth factor receptors, or activation of the phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway [15,16]. Here, MTOR is linked to colonic neoplasm.