Additionally, the NAD+-dependent de-acetylase SIRT1 prevented the CREB-mediated upregulation of KISS1 in a mechanism involving miR-199b. In fact, miR-199b overexpression in CRC represses SIRT1, thus potentiating the CREB-triggered upregulation of KISS1. In this respect, miR-199b could represent a valid prognostic marker or a new possible therapeutic target for patients with CRC due to its ability to modulate the SIRT1/CREB/KISS1 pathway [68]. The gene discussed is KISS1; the disease is colorectal carcinoma.