1/ Any fellow molecular biologists want to attempt answering this question: What is the probability that the tropism of the virus shifts due to vaccine-accelerated Spike evolution leading to binding of novel receptors other than ACE2?
2/ Since vaccine roll out, the Spike ORF has exhibited high mutation rates and entropy. 
3/ If the structure of Spike shifts far enough away where it gains the ability to dock to another transmembrane protein (while maintaining proteolytic conversion via TMPRSS2 or other like protease), the virus could preferentially gain access to other cell/tissue types.
4/ In addition to altering the pathophysiology of the virus, the shift in tropism could change the mode of transmission.
5/ I know other possible entry receptors are under investigation (CD147, CD26, neuropilin-1, ANPEP, ENPEP, AGTR2, etc), but none of these appear to be major routes. But certainly a shift in Spike affinity could change the game with any of these.
6/ One concerning scenario is an enhanced ability to infect certain types of immune cells, imparting the virus with immune evading capabilities.
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