Experimental studies have documented altered expression of Nln in several disease conditions including stroke (Checler, 2014; Rashid et al., 2010, 2014), and suggested its cerebroprotective function via inactivation of bradykinin, substance P, and neurotensin, and formation of angiotensin‐(1‐7) and enkephalins (Jayaraman et al., 2020; Karamyan, 2019). This evidence concerns the gene TAC1 and Stroke.