GH1 and neoplasm: Indirect mechanisms include 1) direct inhibition of IGF-1 gene expression or GH-dependent IGF-1 synthesis in the liver, 2) immunomodulatory effects: inhibition of lymphocyte proliferation, immunoglobulin synthesis, and cluster of differentiation 4+ (CD4+) T cell-derived interferon-γ synthesis, and 3) inhibition of tumor nutrient supply through peritumoral vasoconstriction.