We show that in ARPKD loss of function of human FPC-CTD (patients AR1, AR2, AR3, and AR8: Supplementary Table S1) is associated with aberrant overexpression of MYC in the cystic kidneys, suggesting that FPC functions as a negative regulator of MYC to prevent cystogenesis, as was previously shown for the pro-proliferative STAT3 (Dafinger et al., 2020). The gene discussed is AR; the disease is autosomal recessive polycystic kidney disease.