Animal studies have shown that chronic stress with continuous activation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS) unfavourably alters the TME (tumour microenvironment) in a way that could promote tumorigenesis, invasion, progression, metastasis, and attenuation of systemic therapy effects, including anti-PD-L1 immunotherapy [102–104]. The gene discussed is CD274; the disease is neoplasm.