Importantly, Gal-9 inhibition restores intratumoral T-cell infiltrates in PDA, but this function is impaired in the context of a dectin-1 deletion, suggesting that the dectin-1/Gal-9 interaction is key in reprogramming CD4+ and CD8+ T-cells for regulating tumor progression; thus, highlighting these players as targets in immunotherapy [89]. The gene discussed is CD4; the disease is neoplasm.