While whether FASL mediates immune escape via activation of FAS in lymphocytes remains unclear, our observation for FASL’s capacity in predicting resistance to ICB not only in multiple cohorts and cancer types but at a comparable robustness with established high profile biomarkers (TIDE, IFNG, CD8, and Merck18) [56, 94, 95] strongly supports its potential to assess response following ICB therapy. The gene discussed is FAS; the disease is cancer.