A study by Avin et al. investigated the direct role of FGF23 on skeletal muscle function by assessing markers of cellular proliferation and differentiation in the in vitro mouse cellular model C2C12, showing that increased levels of FGF23, under the experimental testing conditions, may not directly alter skeletal muscle myoblast proliferation, myotube development, or contractility, hypothesizing that other endogenous substances may be required to act in concert with FGF23 to promote muscle dysfunction in hereditary hypophosphatemic rickets [85]. This evidence concerns the gene FGF23 and hypophosphatemic rickets.