Lung Adenocarcinoma (LUAD) is the predominant subtype of lung cancer and a major cause of cancer-related mortality in Australia. Immune checkpoint-based (ICI) therapy was approved for LUAD treatment and exhibited promising results. However, as many as 80% of LUAD patients experience resistance and relapse. ICI leverages the adaptive immune system, but the innate immune system is also critical. IL-1β is a vital immune cytokine and was identified as a significant driver of LUAD progression through the CANTOS trial. Secretion of bioactive IL-1β is predominately regulated by the NLRP-3 inflammasome. The NLRP-3 inflammasome is a crucial immune sensor, however, the mutation in NLRP-3 contributes to autoimmune disorders. Analysis of TCGA LUAD datasets revealed that 16% of LUAD patients had NLRP-3 mutations (predominately gain-of-function (GOF)) and are associated with the shorter survival of LUAD patients. These mutations are assumed to be tumour cell intrinsic. Therefore, we took advantage of the KRAS G12D and P53 f/f (KP) mouse model of LUAD and crossed them with Cre-inducible GOF NLRP-3 (KPNA) and loss of function NLRP-3 (KPN) mice. Strikingly, the genetic ablation of the NLRP-3 significantly increased the overall survival of mice compared to KP and KPNA. To investigate the tumour microenvironment alteration, we performed spatial transcriptomics. ST confirmed the hyper-activation of the Inflammasome pathway and increased gastric transcriptional program in the KPNA model and further validated at the protein level using lineage markers. Moreover, pharmacological inhibition of NLRP-3 suppressed gastric differentiation, and tumor progression in the experimental group compared to the control group. Our data suggests that hyperactivation of NLRP-3 drives LUAD progression, highlighting it as a promising therapeutic target.