On the contrary, the molecular processes in the ST in the case of PD could compensate for any alteration in the SN through demonstrating an opposite pattern of MALAT1 expression similar to what was reported by Cabeza-Arvelaiz et al. about the effect of the upregulation of the human SNCA gene on the ST in a mouse model, which exerted a survival of neurons opposite to what happened in the SN [51]. The gene discussed is SNCA; the disease is Parkinson disease.