Recently, Guenther and colleagues found that IGF-1R overexpression was a resistance mechanism to CDK4/6 inhibitors; a CDK4/6 inhibitor and an IGF-1R inhibitor were synergistic in vitro against ES cells and the combination of these two inhibitors were more effective than single regimen in ES tumor control in mouse models [11]. The gene discussed is IGF1R; the disease is neoplasm.