NLRP3 activators are chemically and structurally different suggesting that they are not directly recognized by the NLRP3 inflammasome. It is more likely that they activate inflammasome indirectly by inducing changes in endogenous proteins that are recognized as danger signals. In addition to cathepsin activity, potassium efflux and ROS production are the common features associated with NLRP3 inflammasome activation. It was very recently shown that thioredoxin-interacting protein links oxidative stress to inflammasome activation [43] . Our proteomic data shows that there is re-localization of mitochondrial proteins to the cytoplasm already at 6 h after influenza A virus infection. These proteins contained several components of the inner mitochondrial membrane including proteins involved in electron transport chain and oxidative phosphorylation. The results suggest that there is a substantial change and/or damage in mitochondrial structure at early phases of influenza A virus infection which may contribute to reactive oxygen species production during infection. This is likely to contribute to the inflammasome activation and apoptosis seen in influenza A virus-infected macrophages. Our current results clearly show that src tyrosine kinase activity is essential for inflammasome activation in response to influenza A virus infection: src kinase specific inhibitors PP2 (Fig. 5 F and G) and src kinase inhibitor II (data not shown) abolished influenza A virusinduced secretion of IL-1b and IL-18. It has also been recently shown that src tyrosine kinase Lyn plays a critical role in the activation of NLRP3 inflammasome in response to malarial hemozoin [44] . Src tyrosine kinases are responsible for the regulation of ROS formation through NADPH oxidase complex [27] . Activation of src tyrosine kinases results in phosphorylation of its substrates Tks4 and Tks5. These proteins act as molecular organizers that specifically activate NADPH oxidases resulting in ROS formation [45] . In conclusion, our results demonstrate a novel link between src tyrosine kinase activity, ROS formation, and inflammasome activation during viral infections.