Enhanced susceptibility to oxidative stress (possibly exacerbated by disease-specific mechanisms in the setting of SLE and CTDs [67] and impaired regulation of IL-16/IL-18-biassed inflammatory responses [68,69] have been proposed as potential distinctive traits of vaccine-associated myocarditis and might account for troponin alterations uncoupled from clinically overt myocarditis relapses in the short- and long-term follow-up of patients receiving mRNA vaccines in the context of cardiac and non-cardiac autoimmunity. This evidence concerns the gene IL16 and systemic lupus erythematosus.