Because the lysis of the T1 tumor target cells by the NK92 clone and by NK cells isolated from healthy donor's is mainly mediated by the Perforin/Granzymes (PFN/Gzms) pathway, as shown by abrogation of NK92 and NKds cytotoxicity after treatment with concanamycin A (CMA) which inhibits cytotoxic granules exocytosis (Supplementary Figure 3A), we also tested whether the CAFs or the NFs CMs alter T1 tumor cell susceptibility to PFN/Granzyme B (GzmB)-induced cell death by measuring the activation of effector caspases in either control or CMs-pre-treated cells. The gene discussed is PRF1; the disease is neoplasm.