We then analyzed the contributions of several well-known chemoresistance-related signaling pathways, specifically cell-adherence molecules (E-cadherin, N-cadherin, and β-catenin), PI3K-related kinases (pAkt/Akt), apoptosis-related molecules (p-Bad/Bad, Bax, and Bcl-2), cyclin-dependent protein (p27), autophagy-related molecules (LC3b and p62) and gap junction (connexin43)-related pathways [16–27], to the density-dependent IC50 variation for cisplatin in ovarian cancer cells (Supplementary Table S8). This evidence concerns the gene BCL2 and ovarian carcinoma.