SSc patients express elevated TGF‐β1 levels in the early lesions, but not in established fibrotic tissue.52 Kim and collaborators demonstrated that TGF‐β1 induced the activation of Akt in normal and RA synovial fibroblasts, and that TGF‐β1 exerted its anti‐apoptotic effect, in part, through the PI3 kinase/Akt pathway.53 Here, AKT1 is linked to systemic sclerosis.