MET and hepatocellular carcinoma: This model has illustrated the vulnerability of specific cells to slightly enhanced RTK levels, notwithstanding the resilience of most cell types.[27, 28, 29] For example, at adulthood enhanced MET levels in the liver trigger spontaneous formation of hepatocellular carcinoma, recapitulating several features of human patients.[29, 30, 31, 32] Here, we report the generation of a unique mouse model (MMTV‐R26Met mice) in which a subtle increase in the expression levels of the wild‐type MET RTK leads to spontaneous TNBC formation.