Preclinical models have also demonstrated that human epidermal growth factor receptor (EGFR) family inhibitors, SHP2 inhibitors, mammalian target of rapamycin (mTOR) inhibitors, and inhibition of CDK4/6 could enhance the anti-tumor activity of MRTX849 and inhibit KRAS-dependent signaling pathways (46). This evidence concerns the gene EGFR and neoplasm.