As a proof of concept, Chen et al. compared the effects of cell-autonomous and systemic Akt1 and Akt2 deletion on mammary tumorigenesis and found that systemic Akt2 ablation did not protect against metastasis, while increased primary tumor development was due to a compensatory rise of systemic insulin levels, which hyperactivates Akt and enables ErbB2 activation. Here, ERBB2 is linked to neoplasm.