The [99mTc]Tc-iFAP uptake in HER2+ could be associated to the Erb2-mediated phosphorylation of Tyr654 of β-catenin, which promotes the activation of Wnt signaling pathways and the consequent promotion of the tumor invasive capacity (FAP expression) through a very common mechanism in breast cancer, the epithelial–mesenchymal transition (EMT) process, induced by the microenvironment, which infers the gain of invasive capacity and the arrest of the cell cycle, while, at the signaling level, it implies the repression of E-cadherin expression through snail/slug [14,15]. The gene discussed is CDH1; the disease is neoplasm.