Consistent with this observation and the results of the in vitro study, ZEB2 knockout in TKI-resistant NSCLC tumor cells hindered the trend of M2 polarization in TAMs, demonstrated by lower percentages of CD206+ TAMs in F4/80+ TAMs, compared with TKI-resistant NSCLC cells treated with LV-shNC, while elevated the level of M1 polarization, evidenced by increasing percentages of CD86+ TAMs in F4/80+ TAMs [Figure 4F and G]. The gene discussed is ZEB2; the disease is neoplasm.