Our data show that in addition to known iCAF drivers such as IL1 [5] and IFNβ [19], IFNγ and TNFα are able to induce a range of cytokines and chemokines associated with an iCAF phenotype in NSCLC patient‐derived CAFs in vitro, which suggests that activated T cells can modulate the CAF secretome. The gene discussed is IL1B; the disease is non-small cell lung carcinoma.