To determine whether GR-mediated regulation of MHC-I is required for the observed anti-tumor effect of GR depletion or inhibition, we knocked down B2M, an essential structural component of the MHC-I complex, in HY24409 cells (Fig. 5a), which abrogated the upregulation of surface MHC-I induced by GR depletion or inhibition (Fig. 5b–e). This evidence concerns the gene B2M and neoplasm.