Hence, the majority of our cases supported the linear progression model (4/6 patients) of metastasis, in which the primary tumour cells diversified over a period of time, gaining several mutations and CNVs including driver events (e.g., TP53, FAT3 and BCORL1) before achieving metastatic potential to migrate and colonise distal sites.48 Linear progression models have overall less heterogeneity and more sharing of mutations between primary and metastatic tumours, as seen in our patients.49 Therefore, targeting trunk alterations in this patient population seems highly desirable. The gene discussed is FAT3; the disease is neoplasm.