Our data, clearly indicating the existence in some TNBC of a Vav1/miR-29b/Akt2 connection able to precisely down-modulate an Akt isozyme crucial for tumor dissemination, may contribute to better classify breast tumors and suggest that therapies aimed to activate the Vav1/miR-29b axis could have great potential for a more personalized therapeutic approach for breast tumors with a triple negative phenotype. This evidence concerns the gene AKT1 and breast neoplasm.