Updated project metadata. Excision of the N-terminal initiator methionine (iMet) from nascent peptide chains is an essential and omnipresent protein modification carried out by Methionine aminopetidases (MetAPs) and accounting for a major source of N-terminal proteoform diversity. While MetAP2 is known to be implicated in processes such as angiogenesis and proliferation in mammals, the physiological role of MetAP1 is much less clear. In this report we studied the omics-wide effects of MetAP1 deletion and MetAP inhibition in general. While the levels of iMet retention are inversely correlated with cellular proliferation rates, deletion of MetAP1 was in part rescued by the increased MetAP2 expression and activity profiles observed.