Blockade of IL6 abrogates immunotherapy toxicity and promotes tumor immunity, showing a higher density of CD4+/CD8+ effector T cells.[280] Ovarian cancer cells overexpressing EGFR enhanced IL6 production and secretion by activating the JAK2/STAT3 signaling.[281] In EGFRmut mouse model (L858R or T790M) and EGFR‐transfected primary human endobronchial cells, IL6 expression was elevated.[282] A similar phenotype was found in the EGFRmut NSCLC tumors with acquired EGFR‐TKI resistance; IL6 is upregulated.[283]. The gene discussed is CD8A; the disease is neoplasm.