Moreover, numerous studies using GH transgenic (hGH or bGH) mice, GHR antagonist (GHA) transgenic mice, congenital and adult-onset GHR knockout (GHRKO, 6mGHRKO) mice and several mouse models of GH deficiency (Ames, Snell, lit/lit) confirm the tumor driving role of GH and IGF1 and also reveal several IGF1-independent actions of GH in favoring a therapy-resistant and metastatic cancer phenotype (7–12). This evidence concerns the gene GHR and neoplasm.