In cancer cells undergoing EMT, experimental inhibition of HA synthesis (e.g., 4-MU) or CD44 silencing (e.g., by RNAi) leads to the suppression of EGFR activity and downstream signaling pathways (ERK, AKT), resulting in the reversal of the EMT phenotype and attenuation of cell invasiveness [218,219,220]. The gene discussed is CD44; the disease is cancer.