The administration of broad-specificity HDACi, targeting class I and II isoforms, has been shown to induce an increase in PD-L1 expression in anaplastic thyroid carcinoma cells [62], while class I-targeting agents have displayed significant potential to upregulate PD-L1 in triple-negative breast carcinoma, head and neck squamous cell carcinoma, NSCLC, and Hodgkin lymphoma [63,64,65,66,67]. This evidence concerns the gene CD274 and triple-negative breast carcinoma.