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While immune-mediated hepatitis results from overactivation of cytotoxic CD8+ T cells, which infiltrate hepatic lobular regions and mediate direct hepatocyte injury, TKI-related hepatic dysfunction is associated with direct hepatic effects from VEGFR inhibition leading to microvascular injury and dysregulation of fibrogenic pathways ( Therefore, attribution of toxicity may require temporary discontinuation of one or both agents, guided by AE severity, followed by close clinical monitoring to assess reversibility

Removal of these environmental cues will result in an enhancement in pharmacologic effect

OncoTargets Ther (2020) 13:1158394

NFATc1, but not NFATc2, is required for CD8 + T cells to engage in the T cell activation-induced metabolic switch to glycolysis [185]

Table S3: Exome versus Sanger sequencing