This study found that FGF23 levels were independently associated with LVH in a non-dialysis dependent CKD population (n = 3070) and induced LVH, both in vitro and in vivo, through the Klotho-independent FGF receptor activation of the phospholipase Cγ/calcineurin/nuclear factor of activated T cell signaling pathway, without activation of PI3K-Akt, a mediator implicated in physiological rather than pathological hypertrophy [65]. Here, FGF23 is linked to chronic kidney disease.