First, we found that some events, such as KRAS amplification, JAK2 amplification, CADM1 deletion, and NFKBIA deletion, were clonal in residual primary tumours but subclonal or undetectable in pretreatment primary tumours, suggesting that these events might be associated with treatment resistance and further metastatic progression (Fig. 2d). The gene discussed is KRAS; the disease is neoplasm.