ERBB2 and infection: As the TKIs inhibit the activity of HER2 [23], to further explore the antiviral mechanism of compound L3, we first used MCF-7 cells that constitutively express endogenous HER2 to investigate whether compound L3 could reduce flaviviral infection by inhibiting endogenous HER2 activity and HER2 downstream signaling molecules, such as Src and ERK1/2 [24,25].