Nuclear factors with significantly altered expression in CMT1A, including Kruppel-like factor 2 (KLF2), cyclic AMP response element-binding protein (CREB1), and signal transducer and activator of transcription 3 (STAT3), potentially show a compensatory state in response to a pro-ferroptotic environment, as all of these transcription factors act as stress regulators and ferroptosis suppressors [60,61,62]. This evidence concerns the gene STAT3 and Charcot-Marie-Tooth disease type 1A.