In our cellular model of tumour cell–fibroblast interaction, there is obviously no consequence for the regulation of the immune response, but we hypothesise that the activation of these pathways, as evidenced by the overexpression of IL-6, LIF, CCL2 and others and the subsequent activation by phosphorylation of STAT3 in BT-474, could be relevant in the acquisition of resistance to anti-HER2 therapy in the tumour cell. The gene discussed is LIF; the disease is neoplasm.