When EGFR was activated, PEDV infection further reduced the fluidity of NHE3, whereas infection with PEDV after inhibition of EGFR activity could enhance the fluidity of NHE3, indicating that during PEDV infection, the stronger the activity of EGFR on the IPEC-J2 cell membrane, the weaker the fluidity of NHE3, i.e., negative feedback by EGFR regulates the fluidity of NHE3 on the plasma membrane. This evidence concerns the gene EGFR and infection.