The changes in the SLM2-mediated splicing of the mRNA regions encoding the PEVK domain and another part of the I-band region of titin, which act as entropic springs mediating flexibility and contractile properties of the heart muscle, suggest that the heart failure-associated up-regulation of SLM2 might be a compensatory mechanism to adapt to the increased wall stress and the hypertrophic response of the heart [46]. The gene discussed is TTN; the disease is heart failure.