FGF23 can also exert cellular effects via αKlotho‐independent mechanisms.74 FGF23 has been shown to stimulate phospholipase Cγ (PLCγ)/calcineurin/nuclear factor of activated T‐cells (NFAT) via FGFR4 in cells that lack αKlotho (Figure 1).74, 75, 76, 77 Such increases in PLCγ/calcineurin/NFAT signaling appear to be important in pathological, as opposed to physiological, cardiac hypertrophy.78, 79 Clearly further mechanistic studies are warranted to delineate mechanisms that can be targeted therapeutically in patients with elevated FGF23 levels. The gene discussed is FGF23; the disease is cardiac hypertrophy.