This study further identified previously unknown off-target interactions of tofacitinib on the TRPM6, with moderate binding affinity. While our computational approach identified TRPC6 and TRPC3 as potential targets, we were unable to experimentally validate these targets due to lack of commercially-available in vitro assays. Thus, we can only speculate that the binding affinity observed with TRPM6 may translate to binding in TRPC6 and TRPC3. Additional experiments are needed to confirm if the C subfamily is also a potential target of tofacitinib. This is important as TRPC6 is known to regulate human clot retraction, physiological hemostasis, and thrombus formation and its inhibition is thought to have a positive effect on thrombotic outcomes.( ) Thus, further research is needed to confirm if there is an off-target activity of tofacitinib-TRPC6.