NALCN and congenital contractures of the limbs and face, hypotonia, and developmental delay: On the other hand, most of the literature seems to indicate that the putative mechanism underlying CLIFAHDD is the gain of function of NALCN explaining the presence of arthrogryposis caused by hyperexcitability of the motor unit, secondary to the depolarization of the resting membrane potential, resulting in a hypercontracted phenotype (Bramswig et al., 2018; Bouasse et al., 2019).