INS and cancer: CDKAL1 has been spotlighted in the association of the SNPs with an increased risk of type II diabetes.[26, 27, 28] Because of the canonical role of CDKAL1 that converts t6A to ms2t6A at the 37th adenosine in tRNALys (UUU), loss of CDKAL1 function results in decreased ms2t6A modification in tRNALys (UUU), leading to a misreading of the lysine codon of the proinsulin gene and decreased insulin secretion.[29] Although many reports have been published on the association of CDKAL1 with diabetes,[38, 39, 40] no biological evidence has linked CDKAL1 to cancer progression.