These results suggest that FHL1 functions as a MAPK scaffold by directly interacting with Raf-1/MEK2/ ERK2 to physically insulate the MAPK pathway to the titin N2B region of the sarcomere in a Gq stimulus-specific manner and efficiently transmit MAPK signals to regulate cardiac hypertrophy (Figure 1). The gene discussed is RAF1; the disease is cardiac hypertrophy.