If we assume that this is indeed the case then the acquisition of the pro-invasive phenotype under these experimental conditions might be explained using a very simplified model in which inhibition of ERα and FASN signalling during hyperglycaemia-induced, matrix-specific EMT triggers the upregulation of caveolin-1 in lipid rafts which in turn activates signalling pathways that lead to increased synthesis and possibly accumulation of cholesterol in a population of residual cancer cells surviving the ERα and FASN knock-down (Fig. 6). The gene discussed is CAV1; the disease is cancer.