Thus, JCPyV could induce a stress response in infected cells resulting in crosstalk between the MEK-ERK MAPK pathway and the p38 MAPK pathway, resulting in activation of SMAD4, which is necessary for infection, yet components of the p38 MAPK pathway may be activated but not play a direct role in JCPyV replication. The gene discussed is MAP2K7; the disease is infection.