RTKs are known to be involved in the development and progression of NAFLD via various pathways such as PI3K/AKT/mTOR, RAS/ERK, Janus Kinase (JAK)/signal transducer and activator of transcription proteins (STAT3), FXR/SHP, etc. These pathways present as cascading signals from RTKs to effector molecules such as nuclear receptors, transcriptional factors or other vital intermediates controlling lipid metabolism, oxidative stress, inflammation and also fibrosis. The gene discussed is STAT3; the disease is metabolic dysfunction-associated steatotic liver disease.