Thus, the dissociated forms of EDS1 and PAD4 are fully competent in signaling receptor triggered localized cell death at infection locations (Rustérucci et al., 2001; Aviv et al., 2002) but, by contrast, an EDS1–PAD4 complex is necessary for basal resistance involving transcriptional up-regulation of PAD4 itself and mobilization of salicylic acid defenses (Rietz et al., 2011). This evidence concerns the gene PADI4 and infection.