This can be a consequence of PD-L1 upregulation [175,176,177], which can occur due to increased JAK-STAT signalling, caused by: loss of the tumour suppressor FBP1 [176,178], mutations in JAK1/2 [179], or stimulation of tumour cells’ interferon-gamma receptor 2 by interferon-gamma released from activated CD8+ T cells in the tumour microenvironment [180,181]. The gene discussed is CD8A; the disease is neoplasm.