A possible mechanistic basis is that these isoforms preferentially generate C16-ceramide, a species implicated in hepatic insulin resistance, steatosis, and inflammation (Chavez and Summers, 2012; Pewzner-Jung et al., 2010) and in the pathogenesis of obesity and type 2 diabetes (Raichur et al., 2019). The gene discussed is INS; the disease is Obesity.