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The findings suggest that erastin can induce ferroptosis in melanocytes, which can be mitigated by N-acetyl-L-cysteine (NAC) treatment, indicating a potential therapeutic approach to protect melanocytes from ferroptosis

This method allows the drug to enter the bloodstream efficiently, ensuring its optimal function

These contradictory findings highlight the need for further investigation to define the physiological role of glucocorticoid signaling in mammalian cardiomyocyte function and regeneration

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Strong pharmacovigilance, physician-led prescribing, patient education, and real-world evidence generation will be critical to sustain long-term trust in this therapeutic class