Apart from BT‐474 cells, showing a luminal B phenotype, in which we confirmed the increase in Akt1 expression as a consequence of Vav1 downmodulation (Grassilli et al., 2014), overexpression of Vav1 reduced p‐Akt1 (Ser473) levels in MCF‐7 cells, showing a luminal A phenotype, and in the HER2‐positive MDA‐MB‐453, allowing to conclude that, in breast tumor‐derived cells and regardless their phenotype, Vav1 is part of signaling pathways ended to modulate the activation status of Akt1. This evidence concerns the gene ERBB2 and breast neoplasm.