Similarly, genetic manipulation of murine liver and gallbladder organoids allowed the investigation of the oncogenic potential of a number of molecular aberrations, showing that KRAS may have a role in tumour initiation, while other alterations, such as PIK3CA mutation and FGFR fusions, occur later in tumour progression and have less tumorigenic potential [13,34]. The gene discussed is KRAS; the disease is neoplasm.