We show that this immune benefit can be further enhanced in a DNGR-1 dependent manner on loss of sGSN, concordant with our previous work showing and increase in tumor-specific T cell responses in GSN-deficient animals.9 Thus, DNGR-1-dependent cross-presentation of dead cell-associated antigens can increase anticancer immunity and could be exploited clinically. This evidence concerns the gene GSN and neoplasm.