In an article by Yachida et al., genetic analysis of a patient's primary and metastatic tumors showed an average of 64% of mutations to be due to founder mutations (present in the original clone) and an average of 36% of mutations to be due to progressor mutations (not present in the original clone) with clonal evolution and metastasis.32 These progressor mutations, such as MYC and KRAS amplification in our case, were not found in the parental clone and can be considered to either be passenger or driver mutations and could have possibly contributed to development of the 2017 tumor. The gene discussed is KRAS; the disease is neoplasm.