Moreover, the activation of GLI increases osteopontin (OPN) to promote a macrophage‐mediated proinflammatory response in a mice model of nonalcoholic fatty liver disease (NAFLD), and Hh signalling promotes M2 polarisation of tumour‐associated macrophages for an immunosuppressive environment, suggesting the Hh pathway is involved in modulating the inflammatory microenvironment [39, 40]. This evidence concerns the gene SPP1 and metabolic dysfunction-associated steatotic liver disease.