Specifically, the authors showed that miR-192 and miR-204 directly suppress HOTTIP in vitro and further identified the GLS1 gene, which plays a critical role in glutaminolysis and tumorigenesis, as a putative downstream target of HOTTIP. Ge et al., thus proposed a novel mechanism of action for HOTTIP, in which it explicates its oncogenic potential by directly upregulating glutaminolysis in HCC cells and promoting cancer cell proliferation in a time and dose dependent manner [136]. Here, HOTTIP is linked to hepatocellular carcinoma.