Van et al. [12] demonstrated that a unique membrane-proximal lysine in the cytoplasmic tail of TRAIL-R1 interacts with MARCH8 which ubiquitinates TRAIL-R1 and thus diminishes its steady-state cell surface expression which suggests MARCH8 as a potential determinant for tumor cell sensitivity to TRAIL receptor-targeted therapy [12]. The gene discussed is MARCHF8; the disease is neoplasm.