INSR and diabetes mellitus: Transcripts, such as cardiac troponin T (TNNT2) (14), muscle-specific chloride channel (CLCN1) (15), insulin receptor (INSR) (16), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (ATP2A1) 1 (17) and several others (18), are mis-spliced, resulting in an imbalance of isoforms which contributes to the DM phenotype.