Like other targeted therapies, cancer cells may also develop resistance to HDAC inhibitors due to, e.g., the use of alternative PTM programs shutting down gene transcription such as DNA methylation [122], the adoption of HSP90-induced unfolded protein response pathway, elevated stress-responsive TF such as NFκB (also named p65), enhanced level of anti-apoptotic proteins such as Bcl-2, and upregulated cellular anti-oxidant signaling [123]. This evidence concerns the gene HDAC9 and cancer.