Previous reports from our laboratory demonstrated that inhibition of HDAC activity with TSA prevent renal cyst formation through targeting MEF2C or Id2 signaling, respectively.[25], [26] Our results that inhibition of HDAC activity with TSA could significantly normalize the mislocalized EGFR from apical to basolateral suggested a third possible mechanism for HDAC in mediating cyst development. This evidence concerns the gene EGFR and cystic kidney disease.