Thus, Snord115 appears largely dispensable for homeostatic feeding and, as such, it considerably differs from Snord116 ablation which leads to decreased body-weight, apparent increased food intake and resistance to HFD-induced obesity, among other phenotypes (Ding et al., 2008; Polex-Wolf et al., 2018; Qi et al., 2016; Skryabin et al., 2007; reviewed in Marty and Cavaillé, 2019). The gene discussed is SNORD116; the disease is obesity disorder.