SEC23B‐deficient T cells have been observed to exhibit accumulation of secreted proteins, proliferative defects and reduced effector functions.[29] SEC24A participates in the ER‐to‐Golgi transport of programmed death ligand 1 (PD‐L1) and stabilizes Golgi residency of PD‐L1, thereby maintaining PD‐L1 expression in tumor cells and resistance to immunotherapy.[30] The wet and highly dynamic environment of the oral cavity often makes local treatment of periodontitis challenging. The gene discussed is SEC24A; the disease is periodontitis.