CD274 and neoplasm: Indeed, Sun et al. developedcompound 11 (HQ-30), an HDACi that bears an N-propyl hydrazide, which induced the degradation of PD-L1 by regulatingcathepsin B (CTSB) in the lysosomes and by enhancing the infiltrationof CD4+ and CD8+ T cells in the tumor microenvironment, thus activatingantitumor immune activity. In particular,compound 11 showed better affinity for HDAC3 since being8-fold more selective over HDAC1 (IC50 = 0.089 μMvs IC50 = 0.730 μM) and more than 100-fold over HDAC6–8.However, data regarding HDAC2 inhibition were missing.