TMPRSS2 and Kallmann syndrome: Naeini et al. proposed that the invasion of the olfactory epithelium by the virus, facilitated by the expression of the angiotensin-converting enzyme 2 (ACE2) receptor and TMPRSS2 enzyme in non-neural olfactory cells, might be a pivotal factor in the development of anosmia, offering a perspective that shifts the focus from sinonasal mucosal involvement to direct viral effects on olfactory tissues [15].