The downregulation of Csa-miR395d-3 and upregulation of eIF2α in SSSL508-28 suggested that the resistant genotype could activate protein synthesis of, for example, receptor-like kinases and receptor-like proteins, at an early stage of infection to restrict the growth of PM pathogens as was reported previously (Tang et al., 2017). The gene discussed is EIF2A; the disease is infection.