Instead of the outdated “two hits” hypothesis which attributes the development of NAFLD to initial steatosis and subsequent systemic inflammation, the novel “multiple parallel hits” hypothesis has proposed various pathogenic factors participating in NAFLD progression parallelly rather than consecutively, including insulin resistance, lipotoxicity, oxidative damage, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, adipose tissue dysfunction, imbalanced innate immunity, cytokine secretion, and the gut-liver axis (3, –, 6). Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.