Lee and coworkers have identified several key factors playing a role in the restoration of EGFR-TKIs sensitivity, such as (i) the metabolic enzyme nicotinamide N-methyltransferase (NNMT) which expression is suppressed by YD in EGFR-TKI-resistant NSCLC cells [75], (ii) the bone morphogenetic protein BMP4 which expression is also drastically reduced in the same cells upon treatment with YD [76] and recently (iii) the anterior gradient protein 2 (AGR2) which is considered a marker of tumor aggressiveness, downregulated by YD in NSCLC-resistant cells [77]. The gene discussed is EGFR; the disease is neoplasm.