Two immunology-centered studies highlight how cancer immune escape can be driven by pathways that extend beyond tumor genetics. German teams reported that aggressive colorectal cancer can evade immune surveillance through WNT signaling–linked mechanisms affecting how tumors respond to immune pressure. Separately, researchers at the University of Pittsburgh reported that T cells expressing the exhaustion marker LAG3 may still shed that marker, exit tumors, and seed long-lasting immune protection, challenging the assumption that exhausted T cells are functionally inert. The findings suggest a more dynamic view of immune persistence after tumor exposure. The combination of studies points to therapeutic strategies that account for immune state transitions—either targeting signaling pathways that shape immune susceptibility or harnessing T-cell plasticity to reduce relapse risk.