Metabolic dysfunction-associated steatotic liver disease (MASLD)-related hepatocarcinogenesis involves metabolic injury, fibrosis, and dysregulated regenerative signaling. Because growth hormone (GH) and insulin-like growth factor 1 (IGF-1) can support repair but also activate proliferative pathways, their effects in advanced disease remain uncertain. We investigated that effect in a MASLD-related HCC model. Male C57BL/6J mice received a Western Diet (WD) and weekly carbon tetrachloride (CCl₄) injections for 24 weeks. At week 16, mice were allocated to untreated or hormone-treated groups, with continuous subcutaneous infusion of IGF-1 at 20 or 60 µg/kg/day or GH at 0.5 or 2 mg/kg/day for 8 weeks. Both hormones reduced serum aminotransferases, lobular inflammation, hepatic collagen and altered selected fibrosis-related transcripts, whereas to IGF-1 20 µg/kg/day and GH 2 mg/kg/day reduced steatosis, and IGF-1 20 µg/kg/day and GH 0.5 mg/kg/day reduced hepatocyte ballooning. GH at 2 mg/kg/day was associated with fewer macroscopically detected hepatic surface nodules, while IGF-1 did not alter nodule burden. The GH 2 mg/kg/day group also showed a lower hepatic p-ERK/ERK ratio. Thus, continuous GH administration during late-stage WD/CCl₄-induced hepatocarcinogenesis was associated with lower hepatic nodule burden. Histopathological confirmation of the lesions and validation in additional models are required before interpreting this finding as an antitumor or therapeutic effect.