Several pathways have been reported to drive the transition of MSCs into CAFs, such as epigenomic reprogramming via lactate in pancreatic cancer (Bhagat et al., 2019), exposure to oxidative stress in breast cancer (Toullec et al., 2010), C-X-C chemokine receptor type 6 (CXCR6) (Jung et al., 2013), and transforming growth factor (TGF)β1 (Barcellos-de-Souza et al., 2016) signaling in prostate cancer, and a supportive role for CD44 in preserving a functional phenotype of CAF has been described (Spaeth et al., 2013). Here, CXCR6 is linked to prostate carcinoma.