Traditionally, programmed cell death (PCD) refers to apoptosis. As such, apoptosis is considered to be the most important cause of hepatocyte death in metabolic-associated fatty liver disease (MAFLD). However, with the discovery of more and more non-apoptotic PCD (including ferroptosis, necroptosis, and pyroptosis), their characteristics which are highly related to inflammation, reactive oxygen species, and immune signal activation have been increasingly valued. A large amount of evidence shows that compared with “immune silence” apoptosis, the non-apoptotic PCD seems to play more critical roles in causing hepatocyte death in MAFLD. The characteristic of pyroptosis is to induce the release of a large number of inflammatory molecules in liver tissue, the characteristic of necroptosis is to lead to complete necrosis of liver cells, and the characteristic of ferroptosis is to have more intense lipid oxidative stress. The purpose of this article is to elaborate the relationship between non-apoptotic PCD and MAFLD, and discuss their possible interaction mechanisms in MAFLD.