The remaining two children were a girl with the de novo mutation c.965T > C (Ile322Thr) in NALCN (sodium leak channel, non-selective) associated with CLIFAHDD syndrome (congenital contractures of the limbs and face with hypotonia and developmental delay syndrome) who debuted with a severe intellectual disability, dystonia, and ataxia at the age of one; and a boy who had a complex movement disorder with a predominance of intentional and postural tremor and had the heterozygous pathogenic variant 619C > T (p.Arg207Trp) in NKX2-1 (NK2 homeobox 1). This evidence concerns the gene NALCN and cerebellar ataxia.