The current model for tumorigenesis is that mutations in genes alter gene expression and/or the normal function of proteins or gene expression. Correspondingly, this predicts that an oncogene such as T antigen would have the same effects in different cell types. However, experiments performed by Mayte Saenz-Robles and colleagues challenge this prediction. In a paper published in Molecular Cancer Research, they describe how a truncated form of T antigen (aka MAMU) called N136 is able to form adenomatous polyps in the digestive tract when expressed in progenitor crypt cells while only causing hyperplasia and dysplasia in the villi. Isn’t cell-type specificity cool?!