Previous studies have shown the involvement of cyclic adenosine monophosphate (cAMP), chemokine, Janus kinase- (JAK-) signal transducer and activator of transcription (STAT), neurotrophin, and hypoxia-inducible factor (HIF) pathways in the initiation and persistence of inflammatory, cancer, and neuropathic pain, as well as their role as pharmacological mediators of analgesic approaches [141, 224, 236–265]. This evidence concerns the gene SOAT1 and cancer.