Along this developmental axis, key immunoregulatory mediators—including IL6ST, LGALS1, STAT1, and TNFRSF6B—were progressively upregulated (Figure 2G), implicating C2_STAT1+ cells as central drivers of immune evasion, therapeutic resistance, and sustained tumor progression in EGFR/TP53 co-mutated NSCLC. The gene discussed is TP53; the disease is neoplasm.