We speculate that, analogues to the impaired hepatic XBP1 function49,50 observed in metabolic disorders, restoration of miR-148a expression under conditions of chronic, un-resolved ER-stress such as obesity and NAFLD/NASH, may present a promising therapeutic strategy to counteract ER-dysfunction, as also proposed by others51. The gene discussed is XBP1; the disease is obesity due to melanocortin 4 receptor deficiency.