A possible inhibition of AS160 - 14-3-3 interaction by Lrrk2 deficiency or/and mutations in LRRK2 and subsequent increased AS160 GAP activity are supposable mechanism for affected insulin-triggered GLUT4 translocation in cells from Lrrk2 deficient animals and Parkinson’s patients with G2019S mutation. This evidence concerns the gene TBC1D4 and Parkinson disease.