Preclinical work by Challita-Eid et al. established that enfortumab vedotin's cytotoxic activity is primarily mediated by this MMAE payload, which can exert potent cytotoxic effects not only in Nectin-4-expressing tumor cells but also potentially in non-tumoral tissues, possibly via target-independent mechanisms or off-target uptake, as indicated by studies on ADCs [7]. The gene discussed is NECTIN4; the disease is neoplasm.