Our study showed that patients with MASLD were characterised by a remarkable increase in the oxidation of ApoC‐III proteoforms compared with controls, that this is a MASLD‐specific process, without a major influence exerted by T2DM (Figure 2), and positively correlated to metabolic features of MASLD (BMI, triglycerides HOMA2‐IR, AST and ALT), and negatively correlated with HDL‐C. The gene discussed is APOC3; the disease is type 2 diabetes mellitus.