Our lab generated CXCL1-Luc2-RFP reporter mouse and its K-rasLA1/+ cross to provide the means for BLI and intravital imaging of spontaneously arising K-ras driven lung tumours, using a transgenic animal model that closely recapitulates human lung tumourigenesis. CXCL1 (KC) chemokine promoter carried by a bacterial artificial chromosome (BAC) was hijacked so as to express reporter proteins, luciferase-2 and RFP, within tumours where oncogenic K-ras is known to drive CXCL1 expression. During this study, we established that CXCL1-Luc2-RFP x K-rasLA1/+ cross does not generate bioluminescence signal, while CXCL1-Luc2-RFP mouse strain is a functional reporter of CXCL1 expression in acute inflammation models. Next, for targeting lung and other cancers, our lab has been studying the activation of Stimulator of interferon genes (STING) as an immunotherapeutic approach. While the direct effects of STING activation have been extensively characterised in antigen presenting cells (APCs), they have not been thoroughly investigated in T cells. We found that in contrast to positive regulation of APCs, stimulation of STING induced T cell apoptosis, which was independent of T cell activation status and potential autocrine type I interferon (IFN) signalling.