Conversely, genetic interventions that enhance the autophagic flux (such as the increased expression of Tfeb) mitigate the induction of NAFLD favored by HFD regimens through activation of PPARGC1A/PGC‐1α (peroxisome proliferative activated receptor, gamma, coactivator 1 alpha) and PPARA/PPARα (peroxisome proliferator‐activated receptor alpha) transcriptional programs (Settembre et al, 2013) and/or through activation of lipophagy (Tanaka et al, 2016). This evidence concerns the gene PPARGC1A and metabolic dysfunction-associated steatotic liver disease.