In contrast, signaling dysregulation, in collaboration with oncogenic pathways such as phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) and Janus kinase (JAK)/ signal transducer and activator of transcription 3 (STAT3), characterizes the CSC niche, particularly in refractory skin cancers [25, 27–29]. The gene discussed is STAT3; the disease is skin neoplasm.