KIT and gastrointestinal stromal tumor: Currently, research indicates that KIT remains the central oncogenic driver even in the later stages of GIST therapy.[25] This study, unlike our study focusing on patients without secondary mutations, demonstrates that AP/AL mutations were rarely observed in progressing GIST samples from the pre‐ripretinib era, but in tumors from patients resistant to ripretinib, AP/AL mutations accounted for 50% of secondary KIT mutations.