Several mechanisms have been proposed to underlie BCa’s diminished responsiveness to cisplatin, encompassing pathways such as Wnt/β-catenin, TGFβ, Ras/MEK/ERK, PI3K/Akt, TNFα/NF-κB, and JAK/STAT, as well as factors such as autophagy, epithelial–mesenchymal transition, cancer stem cells, tumor microenvironment, and epigenetic alterations [39]. The gene discussed is SOAT1; the disease is cancer.