Given the observation of both intermediate fibrosis and intermediate QRS prolongation in Mlc2aCre/+; S1pr1f/+ mice that have no hypertrabeculation, we hypothesize that Mlc2a haploinsufficiency and S1pr1 heterozygosity in cardiomyocytes can lower the threshold for cardiac fibrosis, possibly due to abnormal cardiac mechanics. This evidence concerns the gene S1PR1 and fibrosis.