One such target is cJun; a member of the AP‐1 family of dimeric transcription factors that is overexpressed and upregulated in patient tumor samples in specific cancer types.[8] Further, validation in cancer model systems indicates that cJun inhibition can effectively inhibit tumor progression and proliferation.[9, 10] By binding to 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) response element (TRE) DNA sites (5′‐TGA C/G TCA‐3′), cJun regulates the expression of genes such as CyclinD1, MMP9, and FasL that are involved in differentiation, proliferation, and apoptosis. Here, JUN is linked to neoplasm.