In non-familial RCM, the deposition of amyloid, scleroderma, endomyocardial fibrosis, hyper eosinophilic syndrome, and drug toxicity may promote local inflammation and biomechanical stress to trigger the pathways of Wnt signaling, protein kinase B/phosphoinositide 3-kinase (AKT/PI3K) signaling, Ras-Raf-MEK-ERK, PKC signaling, SMAD, and MAPK [88,89]. This evidence concerns the gene AKT1 and scleroderma.