In EZB-DHITsig+, mutation and deletions are frequently observed in the intracellular death domain of FAS, resulting in apoptotic function loss and further inferior survival [77, 78].Additionally, genetic signatures, which were associated with the depletion of immune and stromal cells and the augment of tumor cells, were enriched in the EZB-DHITsig+ cluster with FAS alteration [78]. The gene discussed is FAS; the disease is neoplasm.