Similarly, in KRAS mutant NSCLC, oncogene activation drives the uptake of amino acids, such as glutamine and leucine in a phosphoinositide 3-kinase (PI3K)/Nuclear factor erythroid 2-related factor 2 (NRF2)/Activating transcription factor 4 (ATF4) dependent mechanism that leads to a pro-oncogenic metabolism reprogramming (87). Here, ATF4 is linked to non-small cell lung carcinoma.