We also applied PDLIM2 global and lung epithelial-specific deletion mice, RelA lung epithelial-specific deletion mice, STAT3 lung epithelial-specific deletion mice, PDLIM2 and RelA or STAT3 double mutant mice, as well as three endogenous (spontaneous, and K-Ras oncogene and carcinogen urethane-induced) and two implanted (syngeneic and xenograft) lung cancer models to examine whether and how PDLIM2 is involved in lung cancer development and responses to anti-PD-1, chemo and epigenetic therapies. This evidence concerns the gene KRAS and lung cancer.