Based on evidence from in vivo translational studies of the involvement of RAF/MEK/ERK and subsequent downstream signaling pathways (such as PI3K/Akt/mTOR and Ca++/Calcineurin/NFAT) on cardiac defects, they have become potential therapeutic targets to treat heart failure in RASopathy patients, both with pharmacological and non-pharmacological therapies (mRNA silencing), focusing on the genotype, which is also useful for predicting the clinical outcome. This evidence concerns the gene AKT1 and RASopathy.