Similarly to what occurred in the xenograft model, combined KRAS G12C and eIF4A inhibitors also caused potent and durable tumor regression in a KRAS G12C–mutant patient-derived xenograft (PDX) model (DFCI-730), with tumors regressing up to 85%–90% in response to the drug combination (Figure 4, C and D). The gene discussed is KRAS; the disease is neoplasm.