Following the initial report, two decades ago, that engagement of CD28 leads to enhanced glycolysis in T cells [2] plethora of data contributed to our current understanding on how metabolic processes are involved in the control of various aspects of T cell signaling, differentiation and pathogenicity allowing for the development of new therapeutic tools or repurposing of already known drugs for the treatment of patients with SLE [3–5]. This evidence concerns the gene CD28 and systemic lupus erythematosus.