CD274 and neoplasm: HITT cooperated with the regulator of G protein signaling 2 (RGS2) to bind to the promoter of PD-L1, leading to decreased PD-L1 translation, which augmented T lymphocyte-mediated cytotoxicity and significantly impeded tumor growth in mouse models, emphasizing the activation of HITT as a promising therapeutic avenue to boost cancer immunotherapy (Lin et al., 2023).