Given that combined V600EBRAF-mTOR inhibition was insufficient to attenuate p-rpS6, and coupled with the observation that PI3K activity and downstream signaling has been proposed as a mechanism of resistance to BRAF inhibition in colorectal cancer [22] and melanoma [23], [24], we evaluated the effects of dual PI3K-mTOR inhibition in COLO 205 cells in conjunction with V600EBRAF inhibition (Fig. 6). The gene discussed is MTOR; the disease is colorectal cancer.