Thus, it would be of interest to further examine whether alterations in DYRK1A-TNNT2 expression in vivo or in more nuanced cellular scenarios such as iPSC cardiomyocytes with trisomy 21 or cells with various degrees of stable DYRK1A over-expression modify Ca2+ handling and beating in response to cardiotoxic insults including anthracyclines. This evidence concerns the gene TNNT2 and trisomy 21.