Second, to investigate the mechanism by which TMEM55B deficiency accelerates MASLD onset and progression to MASH, we performed a series of ex vivo and in vitro studies which support the model that by preventing binding with the adaptor protein JIP4, responsible for facilitating lysosome movement, loss of TMEM55B increased incomplete lipophagic flux and promoted delivery of FA-containing particles to mitochondria, resulting in mitochondrial damage. The gene discussed is PIP4P1; the disease is metabolic dysfunction-associated steatotic liver disease.