Erlotinib (EGFR inhibitor), afatinib (pan-HER inhibitor), and BGJ398 (FGFR inhibitor) showed enhanced anti-tumor effects relative to the monotherapy of ARS-1620, due to their abilities to increase GDP-bound KRAS levels as well as combat negative feedback reactivation of RTKs [85, 103]. The gene discussed is KRAS; the disease is neoplasm.