Thus, although further studies are needed to elucidate the involvement of the p62-based ALIS in the cephalosporin-induced destruction of tubular epithelial cells, our results may provide insight into the pathogenetic mechanisms of the cephalosporin-induced ATN, as one of stress-triggered tissue damage and diseases, by which cephalosporins enriched in the urine undergo massive oxidative stress, leading to tubular epithelial cell parthanatos mediated by the p62-based ALIS. The gene discussed is SQSTM1; the disease is oculocutaneous albinism type 1.