After systemic administration, the siRNA loaded NPs could accumulate in the tumor sites via the enhanced permeability and retention effect.[16] Subsequently, the high concentration of intracellular GSH could destroy the NP structure,[17, 18] thus leading to concurrent scavenging of intracellular GSH and fast release of siAFAP1‐AS1 for efficient gene silencing. This evidence concerns the gene PTGDR and neoplasm.