Is this a cure for XMEN?

In this issue of Blood, Brault et al present exciting new data suggesting that a novel gene editing approach to the treatment of X-linked MAGT1 deficiency with increased susceptibility to Epstein-Barr virus (EBV) infection and N-linked glycosylation defect (XMEN) can restore magnesium transporter expression and natural killer (NK) group 2 member D (NKG2D) expression on CD8(+) T cells and NK cells, thereby restoring their function.

Automated summary

Brault et al present exciting new data suggesting that a novel gene editing approach can restore immune function in patients with X-linked MAGT1 deficiency, increasing their resistance to Epstein-Barr virus infection.