Mutated KRAS contributes to the development of the immunosuppressive TME in PC through several avenues, including recruitment of MDSCs and Treg cells (80, 81), maintenance of the fibroinflammatory stroma (82), induction of Th17 cells (83), and upregulation of PD-L1 expression via mRNA stabilization (84). This evidence concerns the gene KRAS and pachyonychia congenita.