Notably, in the context of skeletal dysplasia mutations such as D333G, the interaction between TRPV4 and RhoA appears to remain largely intact which suggests the gain-of-function of this mutant arises from its intrinsic structural rearrangement, implying a distinct role for TRPV4 itself and the associated elevation of intracellular Ca2+ levels in neuropathy rather than skeletal dysplasia [47]. Here, RHOA is linked to neuropathy.