Future mechanistic studies should evaluate whether targeted depletion of protumor intratumoral consortia, such as Fusobacterium-rich biofilms in colorectal cancer or Veillonella-dominated communities in lung cancer, decreases CAR-T and TIL exhaustion marker expression (PD-1, TIM-3, LAG-3) and enhances immune cell persistence in tumor organoid co-culture and humanized mouse models [126]. This evidence concerns the gene HAVCR2 and lung carcinoma.