Based on our in vitro studies, we hypothesised that using TGF-β inhibitors as therapy would be counterproductive due to the opposite effects of galunisertib on tumour cells (increase in tumour cell growth) versus TME cells (inhibition of CAF functions), while the use of NOX4/NOX1 inhibitors, such as setanaxib, would reduce tumour growth by specifically targeting TGF-β pro-tumorigenic actions in both newly recruited HSC and CAF. The gene discussed is NOX1; the disease is neoplasm.