PDCD1 and neoplasm: We suspect the trend in mortality risk pre- and post-ICI initiation, particularly the worse outcomes near ICI initiation, stems from dose-dependent inhibition of T-cell activation or proliferation in combination with the upregulation of PD-1 or CTLA-4 surface receptors on T-cells by glucocorticoids.26,27 These mechanisms facilitate tumor evasion of immune system surveillance and targeted response.