Men with prostate cancer may be initially responsive to androgen receptor (AR) inhibitors, but in some patients, single-cell RNA-seq of individual CTCs detected heterogeneity in the expression of AR gene mutations and activation of non-canonical (β-catenin-independent) Wnt signaling, which may promote invasiveness and malignant progression, thereby contributing to treatment failure [77]. The gene discussed is AR; the disease is prostate carcinoma.