Consistent with these observations, knockdowns of oncogenic KRAS mutations significantly downregulated the expression of AATs (SLC7A5/LAT1, SLC1A5/ASCT2, and SLC38A2/SNAT2), mTOR activation and cell proliferation by decreasing the l‐glutamine and l‐leucine uptake levels in CRC cells (Fig. 2A–C and Fig. S2). The gene discussed is MTOR; the disease is colorectal carcinoma.