Moreover, in a panel of Non-Small Cell Lung Cancer models, the association of the KRAS G12C inhibitor ARS1620 and a PI3K inhibitor was effective also in models resistant to single agent ARS1620 [34], further reinforcing the concept that using combinations of drugs targeting RAS downstream effectors is not an obsolete therapeutic approach but a challenging path still worthwhile to tread. This evidence concerns the gene KRAS and non-small cell lung carcinoma.