Meibomian gland dysfunction (MGD) is a chronic abnormality of the Meibomian glands (MGs), commonly characterized by terminal duct obstruction and/or changes in gland secretion, which can lead to tear film instability, ocular irritation and ocular surface inflammation [1,2]. In severe cases, it can even cause corneal neovascularization, with the visual impairment seriously affecting a patient's quality of life [3,4]. Worldwide, the incidence of MGD varies significantly, from 3.5% to 69.3% [[5], [6], [7], [8], [9], [10], [11]], with a relatively greater prevalence in Asian populations, ranging from 49.2% to 69.3% [[9], [10], [11]]. Thus, MGD is recognized as one of the most common ocular surface diseases and is undoubtedly one of the major causative factors for dry eye [2,12,13]. Understanding the complex mechanisms behind MGD is crucial for the development of effective diagnostic tools and therapeutic strategies. However, there are a myriad of factors that underlie the pathogenesis of MGD, and these include local, systemic, environmental, surgery-related and medicine-related factors. Accordingly, different models of MGD are required to evaluate the pathological changes caused by different pathogenic factors. In their comprehensive 2020 review article, Sun and associates [14] coherently described the structure, physiology and morphogenesis of MGs and the pathogenesis of MGD. As such, their paper holds significant value to inform and guide fundamental and clinical research in the field of MGs and MGD with its excellent focus on the benefits and limitations of various models. Models developed to study MGD tend to fall into two camps and are either animal-based or reliant on in vitro systems. Here we review the relative benefits and limitations of the various experimental representations of MGD currently available.