The selective and strong inhibition caused in vitro by NSP4114-135 on SGLT1 suggests that, during rotavirus infection in vivo, the newly synthesized glycoprotein NSP4 is released into the intestinal lumen and acts on the SGLT1 protein, hence, directly causing glucose malabsorption and a concomitant inhibition of water reabsorption [7]. Here, SLC5A1 is linked to Rotavirus infection.