The structural activation of STAT3 is a common feature of NSCLC, and it is also considered to play an important role in tumor resistance to conventional and targeted small molecule therapy, especially the rich mutations in the JAK/STAT pathway (Govindan et al., 2012; Looyenga et al., 2012; You et al., 2014). The gene discussed is SOAT1; the disease is neoplasm.