The study further reported aberrant activation of PDGF-signaling pathway in mutant iPSC-CMs to be responsible for the pathologic phenotype, which is rescued by pharmacological and molecular inhibition of PDGF receptor B. In iPSCs derived from an independent proband of LMNA-associated DCM, Siu et al. (2012) found pharmacological inhibition of ERK1/2 pathway with mitogen-activated protein kinase kinase 1/2 inhibitors to attenuate proapoptotic phenotype of DCM iPSC-CMs. This evidence concerns the gene MAP4K1 and familial dilated cardiomyopathy.