The heterogeneous clinical response to targeted therapies observed in BRAFV600E mutant CRC patients has spurred investigation into the molecular basis underlying these differences, which has led to the discovery of two gene expression-based subgroups of BRAFV600E-mutated CRC, one exerting KRAS/AKT pathway activation, mTOR/4EBP deregulation and epithelial–mesenchymal transition (EMT), and the other showing dysregulation of the cell cycle [3]. The gene discussed is AKT1; the disease is colorectal carcinoma.