Tumor immunogenicity is quantified with a novel method, and the resulting tumor immunogenicity score is an effective tumor-inherent biomarker for prediction of response to immune checkpoint inhibitors.

A library of the paired peptide/HLA multimers and artificial APCs allows for construction of a large database of class I-restricted peptides and cognate tumor-reactive TCR genes at an unprecedented scale.

Downregulation of mitochondrial activity by immunosuppressive tumor-derived soluble factors leads to systemic unresponsiveness to the PD-1 blockade therapy.

SLAMF6 is an inhibitory checkpoint of T cells, the lack of which leads to better tumor control, suggesting a new immunotherapy target.

Cancer cell expression of the T-cell co-stimulatory molecule CD80, or treatment with agonistic antibodies targeting the T-cell co-stimulatory receptors OX-40 or 4-1BB, enhances the anti-tumor activity of FAK inhibition.

Tregs form an "immunosuppressive ring" around solid tumors that is broken down during adoptive cell therapy and cyclophosphamide combination immunotherapy.

Long under-appreciated, fibroblast biology is a key aspect of understanding how the immune system responds to tumors and may hold the key to improving immunotherapy in this tricky space.

Engineered T cell receptors enable targeted immunotherapy with a reduced risk of harmful autoimmunity.

Poxin enzymes are a diverse family of insect and viral 2′3′-cGAMP nucleases, which evolved from self-cleaving RNA virus accessory proteases.

Genome-wide CRISPR/Cas9 screens enable the identification of actionable vulnerabilities of oral squamous cell carcinoma, and their unique dependencies on YAP1 and WWTR1 of the Hippo pathway.