Lnc-Tim3 is upregulated in tumor-infiltrating CD8 T cells, inversely correlating with IFN-γ and IL-2 production. It drives CD8 T cell exhaustion and survival by binding to Tim-3, blocking BAT3 interaction, inhibiting Lck/NFAT1/AP-1 signaling, and promoting nuclear Bat3-mediated activation of p300-dependent anti-apoptotic genes (MDM2, Bcl-2). Here, HAVCR2 is linked to neoplasm.