To determine whether the increased Mp/Col15A1 levels could contribute to the DCM phenotype in DM1, we applied our DM1 fly models and performed genetic rescue experiments by attenuating Mp expression in the DCM‐developing Hand > Bru3 context and we used UAS‐UPRT; Bru3 as a negative control (UPRT encodes uracil phospho‐ribosyltransferase enzyme). This evidence concerns the gene COL15A1 and familial dilated cardiomyopathy.