Interestingly, CXCL5 is overexpressed in HCCs with high metastatic potential.30 Zhou et al. showed that the CXCR2/CXCL5 axis contributes to epithelial to mesenchymal transition (EMT) through activating the PI3K/Akt/GSK‐3β/Snail pathway in HCC cells.31 Additionally, CXCL5 is an effector of tumor‐associated neutrophils that mediate the intratumoral infiltration of macrophages and regulatory T cells by secreting CCL2 and CCL17, which enhances HCC progression and sorafenib resistance.32 The gene discussed is SNAI1; the disease is neoplasm.