For instance, a quantitative proteomic approach to assess kinome activity changes in response to MEK inhibition in triple-negative breast cancer (TNBC) cells and in genetically engineered mouse models (GEMMs) [21] allowed showing that MEK inhibition causes acute ERK activity loss, resulting in rapid c-MYC degradation, which in turn induces the expression and activation of several RTKs. Here, MYC is linked to triple-negative breast carcinoma.