Antituberculosis drug-induced liver injury (ATB-DILI) is one of the most significant adverse effects of first-line tuberculosis therapy and a leading cause of treatment discontinuation. Hepatotoxicity associated with isoniazid, rifampicin, and pyrazinamide may substantially impair treatment adherence, prolong treatment duration, and, in severe cases, lead to acute liver failure. This paper provides an overview of contemporary trends in the epidemiology, pathogenesis, diagnosis, and management of ATB-DILI, with particular emphasis on clinically relevant aspects and ongoing controversies. The underlying mechanisms of ATB-DILI origin involve complex interactions between drug metabolism, genetic susceptibility, oxidative stress, mitochondrial dysfunction, and immune-mediated injury, with emerging evidence suggesting a potential role of ferroptosis. Diagnosis relies on biochemical and clinical criteria, the exclusion of alternative causes, and causality assessment tools, such as the Roussel Uclaf Causality Assessment Method – RUCAM scale. Early recognition and timely discontinuation of hepatotoxic agents are of paramount importance, while optimal strategies for treatment reintroduction and the role of hepatoprotective agents are still not fully defined. A better understanding of risk factors and mechanisms, alongside the development of predictive biomarkers and pharmacogenetic approaches, may enable more individualized and safer tuberculosis treatment.