Targeting CCL13 for AD treatment is in its infancy, and an in vitro experiment (8) has pointed out that TNF-α promotes CCL13 gene expression in both IκB dependent and non-dependent pathways by binding to RIP1(receptor interacting protein 1); Non-thermal plasma (NTP) inhibited NF-κB pathway in a non-IκB-dependent manner and downregulated CCL13 expression in AD mice, and the combination of NTP and 1% hydrocortisone cream was found to be more effective. Here, RIPK1 is linked to Alzheimer disease.