Given that ARPDK is genetically inherited kidney diseases that exhibits varying degrees of severity among individuals, several genetic modifiers have been proposed to account for the variability.[33] Our findings suggest that ANKRD26, and likely other TF components/regulators, may act as genetic modifiers of ARPKD and indicate a direct association between TF function and the pathogenesis of ciliopathies beyond PKDs. Here, TF is linked to autosomal recessive polycystic kidney disease.