All these aspects can explain our finding of higher MASLD prevalence in PA compared to MACS, given the direct contribution of aldosterone excess through hepatic MR in regulating gluconeogenesis but also activating proto‐oncogene tyrosine protein kinase, which produces reactive oxygen species (ROS) enhancing proteasome‐dependent degradation of insulin receptor substrate [2]. The gene discussed is INSR; the disease is metabolic dysfunction-associated steatotic liver disease.