In our recent study using genetically engineered mice that exhibit reduced levels of BDNF protein expression such as BDNF heterozygous (BDNF+/−) and proBDNF knock-in (BDNFpro/+) mice, in which the precursor BDNF (proBDNF) is inefficiently converted into the mature form of BDNF, we are the first to demonstrate that the mutant animals spontaneously develop the full spectrum of MASH, including both liver-specific lesions and systemic pathology such as obesity and insulin resistance (Figure 2) [50]. This evidence concerns the gene BDNF and Obesity.