New preclinical data indicate KRAS-mutant tumors rewire adenosine metabolism via NT5E upregulation and ADA suppression, creating an immunosuppressive tumor microenvironment that can blunt immunotherapy responses. Researchers reported reversal potential using ADA nanoparticles, NT5E silencing, or A2AR blockade. The findings point to a concrete, targetable resistance circuit in KRAS-driven malignancies—one that could inform combination trial selection with PD-1 blockade or other checkpoint strategies. In a separate immunotherapy angle, researchers reported that inhibiting FGFR signaling can reduce T-cell exhaustion and repolarize macrophages, improving PD-1 blockade efficacy in microsatellite-stable colorectal cancer models—again emphasizing microenvironment gating over single-agent activity.