At the cellular level, H-Ras-Val12 induced several HF-related phenomena: i) it reduced the L-type Ca++ channel current, and sarcoplasmic reticulum Ca++ uptake [25]; ii) it reduced the expression of SERCA2a and the phosphorylation of phospholamban, leading to diastolic dysfunction [27]. The gene discussed is HRAS; the disease is hydrops fetalis.