Since defective autophagy results in depletion of LC3B, and a decrease in LC3B levels has been already proven to be a driver of caspase 1 activation, thus indicating a shift towards apoptosis and inflammation, it can be well assumed that P2X7r acts as molecular switch crucial for deciding the cell fate also the programmed pathway of cell survival/death in NASH, before it finally moves on to necrotic damage [81]. Here, MAP1LC3B is linked to metabolic dysfunction-associated steatohepatitis.