Macrophages, which are the predominant infiltrating immune cells during myocarditis, were found to respond to CVB3 infection by upregulation of calpain-4; RNA sequencing of CVB3 infected macrophages in vitro revealed predominant enrichment for pathways related to macrophage maturation and interleukin signaling, and loss of calpain-4 reduced IL-1β expression [19]. This evidence concerns the gene IL1B and myocarditis.