Specifically, Dietrich et al. [16] demonstrated that kirsten rat sarcoma (KRAS), an isoform of the RAS family (HRAS, KRAS, and NRAS), is dramatically overexpressed in HCC due to the loss of tumor-suppressive miRNA-622, activating the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) and PI3K/serine/threonine kinase (Akt) signaling pathways and contributing to tumor progression, sorafenib sensitivity, and resistance. This evidence concerns the gene NRAS and neoplasm.