Its resistance mechanism involves intracellular metabolic disorders (Ríos-Luci et al., 2017), activation of STAT3 in signal transduction (Wang et al., 2018), specific tumor microenvironment factors (Endo and Wu, 2021), and overexpression of Polo-like kinase 1 (PLK1) (Ö et al., 2018), among others. The gene discussed is PLK1; the disease is neoplasm.