KRAS and non-small cell lung carcinoma: Notably, the observation that RAS pathway genes (e.g., RTKs, RAS) and downstream effectors (e.g., ERK, phospho-ERK) were not suppressed is consistent with the lack of enhanced suppression of RAS signaling throughout this study and suggests that eIF4A inhibitors do not potentiate the effects of KRAS G12C inhibitors in NSCLC by triggering a deeper suppression of this pathway.