BAX and Zika virus infectious disease: Han et al. (2021) showed that Bax is integral to the mechanism that ZIKV infection induces apoptosis, as siRNA knockdown experiments silencing Bax significantly decreased loss of cell viability following ZIKV infection. This is likely a result of a direct interaction between NS4B and Bax, as NS4B was shown to localise to the mitochondria of infected cells. It has been proposed that NS4B localisation at the outer mitochondrial membrane can trigger the exposure of the N-terminal epitope of Bax, which subsequently destabilises the mitochondrial membrane (Han et al., 2021).