NFATC1 and non-small cell lung carcinoma: In ICI-responsive NSCLC patients, the increased activity of the tryptophan pathway, especially through tryptophanyl-tRNA synthetase (WARS)-mediated tryptophanyl-lysine modification, facilitates hormone receptor interactor 12 (TRIP12)-driven degradation of nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), a PD-1 transcription factor.