In addition to this work, we also demonstrated in a recently characterized new C. elegans model for PD (erals1), which is engineered to express human α-synuclein, that the loss of function of Ife-2, the worm ortholog of ITPKB increases the formation of α-synuclein inclusions in the dendrites of adult animals [23]. This evidence concerns the gene ITPKB and Parkinson disease.