The induction of an immunosuppressive microenvironment orchestrated by KRAS mutants seems to be also dependent on the transcription regulator Yap, due to the observation that Yap ablation in KRAS/TP53 mutant pancreatic cells prevents MDSC recruitment favoring MHCII+ anti-tumor macrophages, resulting in T cell reactivation, apoptosis of neoplastic cells, and tissue regeneration [51]. Here, KRAS is linked to neoplasm.