Specifically, it inhibits Raf kinase, a key component of the RAF/MEK/ERK signaling pathway, along with vascular endothelial growth factor receptors (VEGFR-1, -2, and -3), platelet-derived growth factor receptor-beta (PDGFR-β), and KIT Proto-Oncogene, Receptor Tyrosine Kinase (c-Kit), among others.6 Through this multi-faceted inhibition, sorafenib suppresses tumor growth, vascularization, and metastatic potential, making it a valuable therapeutic agent in HCC management.7 Despite its clinical relevance, sorafenib’s therapeutic benefit is often compromised by the rapid emergence of resistance. The gene discussed is KIT; the disease is neoplasm.