To further explore the mechanisms involved in PYCR1-regulated proliferation, drug resistance, and EMT when PYCR1 was knocked down in colorectal cancer cells, the researchers observed that the STAT3-mediated p38 MAPK and NF-κB signaling pathways were inhibited, while a simultaneous overexpression of STAT3 could partially reverse the effects of PYCR1 on colorectal cancer cell proliferation, drug resistance, and EMT (31). The gene discussed is PYCR1; the disease is colorectal cancer.