Researchers have identified the gene SDR42E1 as a critical regulator of how the body absorbs and metabolises vitamin D, and shown that disabling the gene sharply curbs the survival of colorectal cancer cells. The work, published in Frontiers in Endocrinology, used CRISPR/Cas9 to switch off SDR42E1 in the HCT116 cancer-cell line, reducing cell viability by 53 percent. Loss of SDR42E1 altered expression of 4,663 other genes tied to cancer signalling and sterol metabolism, underscoring the gene’s role as a molecular hub. Because healthy tissue relies less on SDR42E1, the authors say selectively blocking the protein could kill tumour cells while sparing surrounding tissue. Lead author Nagham Nafiz Hendi of Middle East University and corresponding author Georges Nemer of Hamad Bin Khalifa University caution that extensive validation is still needed before the approach can enter the clinic. Even so, they argue that modulating SDR42E1—either inhibiting it in tumours or boosting it in disorders linked to vitamin-D deficiency—opens “new potential avenues” for precision oncology and other metabolic diseases.