Several preclinical studies have shown that mutant KRAS can induce the conversion of conventional anti-tumorigenic CD4+FoxP3- T cells to pro-tumorigenic CD4+FoxP3+ Tregs through the secretion of IL-10 and TGF-β via the MEK–ERK–AP1 axis activation in NSCLC, PDAC and CRC models,225,241,242 highlighting the importance of KRAS signaling in producing an immunosuppressive TIME. The gene discussed is FOXP3; the disease is non-small cell lung carcinoma.