We conducted the two rapamycin screens concurrently, with the expectation that genes identified in one strain background might suppress in the other background. This expectation was based on our previous finding that YPT6 suppressed the autophagy defect of the arl1Δ strain (Yang and Rosenwald 2016). We expected that IVY1 and ATG5 would also suppress the arl1Δ strain’s autophagy defect because, based on our results, we hypothesized that Ivy1 and Atg5 function downstream of Ypt6. However, we found that, other than YPT6 itself, none of the genes identified as suppressors of one strain suppressed the other strain. In other words, COG4, TAX4, and SNX4 selected from the screen of the arl1Δ strain only suppressed the autophagy defect in the arl1Δ strain, not the ypt6Δ strain, whereas IVY1 and ATG5 only suppressed the defect in the ypt6Δ strain, not the arl1Δ strain. Previously, we showed Arl1 and Ypt6 work together to mediate autophagy, as the conditional knockout of both the ARL1 and YPT6 genes can lead to a complete block of autophagy, even at 30°. The fact that they do not share the same set of high copy suppressors may suggest that they have independent roles in some aspects of autophagy as well. Moreover, the fact that SLT2 and PEP3 are rapamycin sensitivity suppressors but cannot suppress the autophagy defects in the arl1Δ or ypt6Δ strain may suggest that Arl1 and Ypt6 regulate TORC1 function; however, at this point, we cannot rule out the possibility that SLT2 and PEP3 are bypass suppressors of the loss of ARL1 and YPT6, respectively.