Modification of RNA with N-methyladenosine (mA) has gained attention in recent years as a general mechanism of gene regulation. In the liver, mA, along with its associated machinery, has been studied as a potential biomarker of disease and cancer, with impacts on metabolism, cell cycle regulation, and pro-cancer state signaling. However these observational data have yet to be causally examined For example, neither perturbation of the key mA writers and , nor the mA readers and have been thoroughly mechanistically characterized as they have been . To understand the functions of these machineries, we developed mouse models and found that deleting led to progressive liver injury characterized by nuclear heterotypia, with changes in mRNA splicing, processing and export leading to increases in mRNA surveillance and recycling.