This important negative result has important implications: (1) different pathophysiological mechanisms likely operate in fatty liver disease initiation (e.g. gain of function in GPAM) and progression driving stage‐specific selective advantage (e.g. loss of function); (2) genetic risk scores capturing only germline variation will not include the pathogenicity conveyed by these regions and additional strategies may be needed to understand the prognostic implications of these somatic mutations. This evidence concerns the gene GPAM and fatty liver disease.