Left: AIC often begins as early, subclinical myocardial injury that may progress toward overt chronic dysfunction, typically marked by a decline in left ventricular ejection fraction (LVEF). Elevations in cardiac troponin are frequently observed shortly after anthracycline exposure and reflect early cardiomyocyte injury. Myocardial edema and inflammation have been detected both in patients and in preclinical models, suggesting that inflammatory activation may occur at an early stage. Electrophysiological changes, including QT interval prolongation, point to early disruption of cardiac ion channel function. Advanced noninvasive imaging tools, such as global longitudinal strain (GLS) and cardiac magnetic resonance (CMR), enable detection of subtle myocardial dysfunction before structural deterioration becomes clinically evident. Timely identification through these advanced tools is essential to intervene before irreversible myocardial remodeling takes place. Right: Oxidative stress, mitochondrial damage, and apoptosis are well-established mechanisms of AIC. Multiomic approaches, including single-cell and spatial transcriptomic as well as epigenomic profiling, have begun to reveal complex transcriptional reprograming impacting key pathways of metabolism, inflammation, and structural homeostasis. These approaches also underscore a central role of intercellular crosstalk perturbations in driving long-term toxicity. Together, this emerging framework may support a more integrated understanding of anthracycline cardiotoxicity and guide the development of targeted interventions.