AKT1 and neoplasm: Subsequently, ZIP5 overexpression enhanced cellular zinc content, thereby diminishing the DNA damage from radiotherapy.596 Additionally, radiotherapy resistance is a major barrier limiting the favorable prognosis in NPC as it may lead to tumor recurrence.597 Zeng et al. found that raised ZIP4 expression activated the PI3K/AKT pathway to induce EMT in NPC cell line C666-1.77 Accordingly, ZIP4 inhibition augmented radiation-induced apoptosis of C666-1 cells ex vivo and in vivo.