Supporting a crosstalk between the Hippo and PI3K pathways in NAFLD-HCC progression, liver-specific deletion of SAV1 promoted fibrogenesis and accelerated hepatocarcinogenesis in PTEN KO mice while SAV1 and PTEN are downregulated in nonviral HCC cases from the TCGA [70]. The gene discussed is SAV1; the disease is metabolic dysfunction-associated steatotic liver disease.