The ability of FASN inhibition to stably impose mesenchymal-like BC tissues to undergo the inverse plastic change that generates epithelial tissue in vivo (Figures 2–4), together with the fact that transient knockdown of FASN was sufficient to suppress hallmark structural and cytosolic/secretive proteins (vimentin, N-cadherin, fibronectin) in a model of EMT-induced CSC-like cells, strongly suggest that FASN signaling might play an unforeseen regulatory role in the structural configuration of the cytoskeleton and, hence, in determining the robustness of EMT vs. MET cell states (Figure 5). This evidence concerns the gene FASN and breast cancer.