Based on our previous findings in prostate cancer cells [15], as well as findings of the current study on HL-60 cells, we postulate that several pathways influenced by 1,25(OH)2D3 may contribute to the observed TXNIP regulation, such as regulation of metabolism-associated signaling molecules, namely AMPK, as well as the modulation of protein stability/degradation. This evidence concerns the gene TXNIP and prostate cancer.