Whilst ASK1 is primarily activated in response to oxidative stress, other factors such as calcium overload, endoplasmic reticulum stress, infection, and receptor-mediated inflammatory signals, including lipopolysaccharide (LPS) and tumour necrosis factor (TNF) can also induce ASK1 signalling (reviewed in Shiizaki [28]). This evidence concerns the gene MAP3K5 and infection.