It has been further suggested that the possible mechanisms of cisplatin resistance development potentially include the abnormal activation of (i) the DNA repair system (such as actin-like 6A and nucleotide excision repair proteins) [38,39]; (ii) downstream signaling molecules (such as EGFR) [7,31]; and (iii) cancer stem cell-like characters (many stemness markers identified in earlier studies and our present study) [17,19,20]. This evidence concerns the gene ACTL6A and cancer.