However, in those established models from pretreated patients where the GIST PDX model only harbors imatinib-sensitive primary KIT mutations (such as UZLX-GIST41), the resistant subclones that required selective TKI pressure in the patient to overgrow sensitive subclones have probably, in turn, been overgrown by TKI-sensitive subclones after absence of this TKI pressure in our mice (Kang et al., 2013; Grunewald et al., 2014). This evidence concerns the gene KIT and gastrointestinal stromal tumor.