IFNG and neoplasm: Because PD-L1-negative HAP1 cells can acquire high levels of cell surface-associated PD-L1 after exposure to IFNγ [57] –a key inflammatory cytokine secreted by T cells and NK cells that operates as the most well-known factor that induces PD-L1 in tumor cells [58–60]–, they provide an idoneous in vitro model to study whether FASN signaling is a regulator of PD-L1-driven adaptive immune resistance [61, 62].