AR and skin squamous cell carcinoma: Towards this goal, we started by comparing the global transcriptomic profiles of (i) multiple CAF strains derived from skin squamous cell carcinomas (SCCs) versus matched normal fibroblasts (NFs) of surrounding unaffected skin;17 (ii) the profiles of human dermal fibroblasts (HDFs) plus/minus androgen receptor (AR) gene silencing, which elicits early steps of CAF activation;13 (iii) the profiles of different CAF strains plus/minus treatment with the bromodomain and extra terminal protein (BET) inhibitor JQ1, which can restore AR expression and reverts the CAF phenotype26.