In line with these observations, TCR diversity and mutation/neoantigen load have been inversely correlated, but both active and suppressive TME immune components, such as Treg and CD8+ T-cells, were present and equally balanced suggesting a scenario where activated anti-tumor CD8+ T-cells are counteracted by pro-tumoral immune suppressive molecules and Treg cells [96] or activated CD8+ T and CD4+ T-helper cells displaying phenotypic markers of exhaustion including PD-1, TIM-3, and LAG3 positivity [30]. The gene discussed is CD4; the disease is neoplasm.