On the one hand, excessive ectopic lipid accumulation and insulin resistance unify MAFLD and CKD pathogenesis, promoting their oxidative stress, inflammation, and fibrosis through shared pathways, such as dyslipidemia induced by the impairment of related enzymes and receptors, activation of inflammatory signals mediated by cell senescence, ALEs, ox-LDL, CD36, and RAGE/TLR-4, and insulin signaling impairment driven by PPAR signals and LCFA/DAG/ceramide. This evidence concerns the gene PPARA and metabolic syndrome.