We demonstrate that soluble recombinant CRTAC1 interacts with insolubilized recombinant CFP and propose that decreases of CRTAC1 associated with severe COVID‐19 result from increased turnover due to activation of the alternate complement pathway as well as to loss of production of CRTAC1 by dying or de‐differentiated T2AE cells. The gene discussed is CFP; the disease is COVID-19.