However, given the pan-neuronal expression of MYT1L, one can wonder if certain subtypes of neurons could be more sensitive to the loss of MYT1L, with distinct cell types leading to each of the diverse panel of clinical phenotypes such as obesity, white-matter thinning, hyperactivity, and social deficits. This evidence concerns the gene MYT1L and obesity due to melanocortin 4 receptor deficiency.