In order to distinguish between FGF23-mediated cardiac hypertrophy via induction of calcineurin/NFAT pathway or activation of RAAS, we stimulated NRVM with FGF23 in the presence and absence of calcineurin inhibitor cyclosporine A (CsA), angiotensin receptor blocker losartan (Los) and steroidal mineralocorticoid receptor (MR) antagonist spironolactone (Spiro) followed by quantification of cardiomyocyte cell size as demonstrated by fluorescent-labeled sarcomeric α-actinin staining and expression of prohypertrophic NFAT target genes. The gene discussed is FGF23; the disease is cardiac hypertrophy.